HCSGD entry for IL6

1. General information

Official gene symbol	IL6
Entrez ID	3569
Gene full name	interleukin 6 (interferon, beta 2)
Other gene symbols	BSF2 HGF HSF IFNB2 IL-6
Links to Entrez Gene	Links to Entrez Gene

2. Neighbors in the network

This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID	GO term	Evidence	Category
GO:0001781	Neutrophil apoptotic process	IDA IEA	biological_process
GO:0002384	Hepatic immune response	IDA TAS	biological_process
GO:0002446	Neutrophil mediated immunity	IC	biological_process
GO:0002548	Monocyte chemotaxis	IC	biological_process
GO:0002675	Positive regulation of acute inflammatory response	IDA	biological_process
GO:0002690	Positive regulation of leukocyte chemotaxis	IC	biological_process
GO:0005125	Cytokine activity	IDA IEA NAS	molecular_function
GO:0005138	Interleukin-6 receptor binding	IEA IPI NAS	molecular_function
GO:0005515	Protein binding	IPI	molecular_function
GO:0005576	Extracellular region	IEA TAS	cellular_component
GO:0005615	Extracellular space	IDA IEA	cellular_component
GO:0005896	Interleukin-6 receptor complex	IDA	cellular_component
GO:0006469	Negative regulation of protein kinase activity	IEA	biological_process
GO:0006953	Acute-phase response	TAS	biological_process
GO:0006954	Inflammatory response	IDA	biological_process
GO:0006955	Immune response	IEA	biological_process
GO:0006959	Humoral immune response	IC	biological_process
GO:0007568	Aging	IEA	biological_process
GO:0008083	Growth factor activity	IDA	molecular_function
GO:0008284	Positive regulation of cell proliferation	IDA IMP	biological_process
GO:0008285	Negative regulation of cell proliferation	IEA	biological_process
GO:0008360	Regulation of cell shape	IEA	biological_process
GO:0009408	Response to heat	IEA	biological_process
GO:0009409	Response to cold	IEA	biological_process
GO:0009611	Response to wounding	IEA	biological_process
GO:0009612	Response to mechanical stimulus	IEA	biological_process
GO:0009897	External side of plasma membrane	IEA	cellular_component
GO:0010574	Regulation of vascular endothelial growth factor production	IDA	biological_process
GO:0010888	Negative regulation of lipid storage	NAS	biological_process
GO:0016049	Cell growth	IEA	biological_process
GO:0019221	Cytokine-mediated signaling pathway	IDA	biological_process
GO:0030168	Platelet activation	TAS	biological_process
GO:0031000	Response to caffeine	IEA	biological_process
GO:0031018	Endocrine pancreas development	IEA ISS	biological_process
GO:0031175	Neuron projection development	IMP	biological_process
GO:0031667	Response to nutrient levels	IEA	biological_process
GO:0032494	Response to peptidoglycan	IEP	biological_process
GO:0032496	Response to lipopolysaccharide	IEA	biological_process
GO:0032722	Positive regulation of chemokine production	IDA IMP	biological_process
GO:0032755	Positive regulation of interleukin-6 production	IDA	biological_process
GO:0032868	Response to insulin	IEA	biological_process
GO:0032966	Negative regulation of collagen biosynthetic process	IDA	biological_process
GO:0033138	Positive regulation of peptidyl-serine phosphorylation	IDA	biological_process
GO:0033160	Positive regulation of protein import into nucleus, translocation	IEA	biological_process
GO:0042102	Positive regulation of T cell proliferation	IDA	biological_process
GO:0042110	T cell activation	IEA	biological_process
GO:0042493	Response to drug	IEA	biological_process
GO:0042517	Positive regulation of tyrosine phosphorylation of Stat3 protein	IDA IEA	biological_process
GO:0042832	Defense response to protozoan	IEA	biological_process
GO:0043065	Positive regulation of apoptotic process	IDA	biological_process
GO:0043066	Negative regulation of apoptotic process	IDA	biological_process
GO:0043154	Negative regulation of cysteine-type endopeptidase activity involved in apoptotic process	IEA	biological_process
GO:0043200	Response to amino acid	IEA	biological_process
GO:0043410	Positive regulation of MAPK cascade	IDA	biological_process
GO:0045079	Negative regulation of chemokine biosynthetic process	IEA ISS	biological_process
GO:0045188	Regulation of circadian sleep/wake cycle, non-REM sleep	IEA	biological_process
GO:0045429	Positive regulation of nitric oxide biosynthetic process	IEA	biological_process
GO:0045454	Cell redox homeostasis	IEA	biological_process
GO:0045599	Negative regulation of fat cell differentiation	NAS	biological_process
GO:0045630	Positive regulation of T-helper 2 cell differentiation	IEA	biological_process
GO:0045666	Positive regulation of neuron differentiation	IEA	biological_process
GO:0045669	Positive regulation of osteoblast differentiation	TAS	biological_process
GO:0045721	Negative regulation of gluconeogenesis	IEA	biological_process
GO:0045727	Positive regulation of translation	IDA	biological_process
GO:0045740	Positive regulation of DNA replication	IEA	biological_process
GO:0045765	Regulation of angiogenesis	IC	biological_process
GO:0045893	Positive regulation of transcription, DNA-templated	IDA	biological_process
GO:0045944	Positive regulation of transcription from RNA polymerase II promoter	IDA IEA	biological_process
GO:0046427	Positive regulation of JAK-STAT cascade	IDA	biological_process
GO:0046677	Response to antibiotic	IEA	biological_process
GO:0046716	Muscle cell cellular homeostasis	IEA	biological_process
GO:0046849	Bone remodeling	IEA	biological_process
GO:0046888	Negative regulation of hormone secretion	IEA	biological_process
GO:0048635	Negative regulation of muscle organ development	IEA	biological_process
GO:0048661	Positive regulation of smooth muscle cell proliferation	IDA	biological_process
GO:0050679	Positive regulation of epithelial cell proliferation	IEA	biological_process
GO:0050710	Negative regulation of cytokine secretion	IEA	biological_process
GO:0050731	Positive regulation of peptidyl-tyrosine phosphorylation	IDA	biological_process
GO:0050829	Defense response to Gram-negative bacterium	IEP	biological_process
GO:0050830	Defense response to Gram-positive bacterium	IEP	biological_process
GO:0050871	Positive regulation of B cell activation	IDA	biological_process
GO:0051024	Positive regulation of immunoglobulin secretion	IDA	biological_process
GO:0051091	Positive regulation of sequence-specific DNA binding transcription factor activity	IDA	biological_process
GO:0051092	Positive regulation of NF-kappaB transcription factor activity	IDA	biological_process
GO:0051384	Response to glucocorticoid	IDA	biological_process
GO:0051592	Response to calcium ion	IEA	biological_process
GO:0051602	Response to electrical stimulus	IEA	biological_process
GO:0051607	Defense response to virus	IDA	biological_process
GO:0051897	Positive regulation of protein kinase B signaling	IEA	biological_process
GO:0051971	Positive regulation of transmission of nerve impulse	IEA	biological_process
GO:0060445	Branching involved in salivary gland morphogenesis	IEA	biological_process
GO:0060664	Epithelial cell proliferation involved in salivary gland morphogenesis	IEA	biological_process
GO:0070091	Glucagon secretion	IEA ISS	biological_process
GO:0070102	Interleukin-6-mediated signaling pathway	IDA IEA	biological_process
GO:0070301	Cellular response to hydrogen peroxide	IDA	biological_process
GO:0070374	Positive regulation of ERK1 and ERK2 cascade	IEA	biological_process
GO:1901215	Negative regulation of neuron death	IEA	biological_process
GO:2000366	Positive regulation of STAT protein import into nucleus	IC	biological_process
GO:2000676	Positive regulation of type B pancreatic cell apoptotic process	TAS	biological_process

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4. Expression levels in datasets

Meta-analysis result

p-value up	p-value down	FDR up	FDR down
0.0001505908	0.2076221686	0.0350769912	0.8831011472

Individual experiment result
( "-" represent NA in the specific microarray platform )

Data source	Up or down	Log fold change
GSE11954	Down	-1.4782073252
GSE13712_SHEAR	Up	1.4502437484
GSE13712_STATIC	Up	0.9362368675
GSE19018	Down	-1.7917354220
GSE19899_A1	Up	2.0701589521
GSE19899_A2	Up	6.0787829505
PubMed_21979375_A1	Up	5.3004054702
PubMed_21979375_A2	Up	4.8924272755
GSE35957	Up	0.6178528025
GSE36640	Down	-1.6771488894
GSE54402	Up	0.5985255884
GSE9593	Up	0.2590431963
GSE43922	Up	2.6253767936
GSE24585	Up	0.3866175714
GSE37065	Up	0.8423835055
GSE28863_A1	Up	0.1024113244
GSE28863_A2	Up	0.5800866567
GSE28863_A3	Down	-0.1568844974
GSE28863_A4	Down	-0.2268380106
GSE48662	Up	0.0013063834

5. Regulation relationships with compounds/drugs/microRNAs

Compounds

Not regulated by compounds

Drugs

Name	Drug	Accession number
Ginseng	DB01404	-
YSIL6	DB05017	-
AV411	DB05066	-
681323	DB05250	-
VX-702	DB05470	-
CRx-139	DB05744	-
HMPL-004	DB05767	-
Siltuximab	DB09036	-

MicroRNAs

mirTarBase

MiRNA_name	mirBase ID	miRTarBase ID	Experiment	Support type	References (Pubmed ID)
hsa-let-7a-5p	MIMAT0000062	MIRT005420	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	19878981
hsa-miR-26a-5p	MIMAT0000082	MIRT007374	Luciferase reporter assay	Functional MTI	23389848
hsa-miR-335-5p	MIMAT0000765	MIRT016949	Microarray	Functional MTI (Weak)	18185580
hsa-miR-365a-3p	MIMAT0000710	MIRT020073	Reporter assay	Functional MTI	21518763
hsa-miR-155-5p	MIMAT0000646	MIRT021049	Proteomics	Functional MTI (Weak)	20584899
hsa-miR-155-5p	MIMAT0000646	MIRT021049	Proteomics	Functional MTI (Weak)	18668040
hsa-miR-124-3p	MIMAT0000422	MIRT022183	Microarray	Functional MTI (Weak)	18668037
hsa-miR-1	MIMAT0000416	MIRT023501	Microarray	Functional MTI (Weak)	18668037
hsa-miR-98-5p	MIMAT0000096	MIRT027449	Microarray	Functional MTI (Weak)	19088304

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mirRecord

No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 143 abstracts the gene occurs.

PubMed ID of the article	Sentenece the gene occurs
27917303	Then, the effect of synthetic miR-146a mimetic on IL-6 and VEGF-A expression was analyzed in RPE cells treated with and without TNF-alpha
27917303	Overexpression of miR-146a by miRNA mimics inhibited VEGF-A and TNF-alpha-induced IL-6 expression
27899899	Moreover, in the first passages, MSCs were capable to release IL1beta, IL6, and IL8, as well as to produce active MMPs allowing them to migrate
27883166	Serum interleukin-6 decreased (2
27329245	In a study of SASP markers, the expressions of IL6 and IL8 were also more upregulated in human non-pathological prostatic glands after ADT than in untreated specimens
27329245	IL6, IL8, and MMP2 were expressed more strongly in human prostate cancer specimens resected after ADT than in untreated tumors
27266474	C-reactive protein, interleukin-6, waist circumference, triglycerides, high-density lipoprotein cholesterol and cigarette smoking were significant mediators in the relationship between psychopathology and LTL
27197269	Correction: Radiation-Induced Loss of Salivary Gland Function Is Driven by Cellular Senescence and Prevented by IL6 Modulation
27146058	Moreover, compared with HSC(+/+), HSC(-/-) showed high expression of Il-6 and chemokine mRNA when cocultured with mouse Hepa 1-6 cells
27115165	Expressions of IL-6 and IL-8 in RPE/choroid were analyzed using RT-PCR
27115165	Expressions of proinflammatory IL-6 and IL-8 were significantly upregulated in RPE/choroid of aged SAMP8 mice
27106773	To evaluate the expression of markers correlated with cellular senescence and DNA damage (8-hydroxy-2'-deoxy-guanosine (8-OHdG), p53, p21, APE1/Ref-1 (APE1), interleukin (IL-6 and IL-8) in placentas from healthy and pathologic pregnancies
27106773	In this study, we demonstrated a significant influence of gestational age on the expression in the trophoblast of 8-OHdG, p53, p21, APE1, and IL-6
27106773	In placentas of cases affected by PE, HELLP, or IUGR, there was an increased expression of 8-OHdG, p53, APE1, and IL-6 compared to controls (only IL-8 was significantly decreased in cases)
27106773	Placentas from pathological pregnancies had an altered expression of 8-OHdG, p53, p21, APE1, IL-6, and IL-8
27041570	We demonstrate that ectopic expression of HOTAIR induces NF-kappaB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kappaB target genes
26943583	A three-pronged approach has been adopted to assess the if adalimumab is able to: i) modulate a panel of classic and novel senescence- and SASP-associated markers (interleukin [IL]-6, senescence associated-beta-galactosidase, p16/Ink4a, plasminogen activator inhibitor 1, endothelial nitric oxide synthase, miR-146a-5p/Irak1 and miR-126-3p/Spred1) in human umbilical vein endothelial cells (HUVECs); ii) reduce the paracrine effects of senescent HUVECs' secretome on MCF-7 breast cancer cells, through wound healing and mammosphere assay; and iii) exert significant decrease of miR-146a-5p and increase of miR-126-3p in circulating angiogenic cells (CACs) from psoriasis patients receiving adalimumab in monotherapy
26943583	TNF-alpha blockade associated with adalimumab induced significant reduction in released IL-6 and significant increase in eNOS and miR-126-3p expression levels in long-term HUVEC cultures
26934440	Increased IL-6 secretion by aged human mesenchymal stromal cells disrupts hematopoietic stem and progenitor cells' homeostasis
26934440	IL-6 neutralization restores the MSC-HPSC crosstalk in senescent and adult MSC-HSPC co-cultures highlighting the relevance of the local microenvironment in maintaining HSPC homeostasis
26924930	In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions
26759233	Radiation-Induced Loss of Salivary Gland Function Is Driven by Cellular Senescence and Prevented by IL6 Modulation
26759233	Importantly, using IL6 knockout mice, we found that sustained expression of IL6 in the salivary gland long after initiation of radiation-induced DNA damage was required for both senescence and hypofunction
26759233	Additionally, we demonstrate that IL6 pretreatment prevented both senescence and salivary gland hypofunction via a mechanism involving enhanced DNA damage repair
26759233	Collectively, these results indicate that cellular senescence is a fundamental mechanism driving radiation-induced damage in the salivary gland and suggest that IL6 pretreatment may represent a promising therapeutic strategy to preserve salivary gland function in head and neck cancer patients undergoing radiotherapy
26677981	Cytokine profiling revealed that miR-34a significantly modulated IL-6 and -8 production, which was strongly related to cellular senescence
26658759	Further, geranylgeranyl transferase, Rac1 or Cdc42 depletion reduced IL-6 secretion by senescent cells
26654980	Senescent cells upregulated the proinflammatory cytokines IL-6 and IL-8, the main markers of the senescence-associated secretory phenotype (SASP)
26629698	Cellular senescence is defined as an irreversible cell cycle arrest and is associated with the release of molecules known as the senescence-associated secretory phenotype that can selectively promote the growth of pre-neoplastic keratinocytes (osteopontin) and cancer invasion (transforming growth factor beta, matrix metalloproteinases, interleukin 6 and lactate)
26521742	Systemic inflammation can be promoted by aging changes in adipose tissue that result in increased production of cytokines such as interleukin (IL)-6 and tumor necrosis factor-alpha (TNFalpha)
26521742	Numerous studies have shown an age-related increase in blood levels of IL-6 that has been associated with decreased physical function and frailty
26521742	Importantly, higher levels of IL-6 have been associated with an increased risk of knee OA progression
26521742	However, knockout of IL-6 in male mice resulted in worse age-related OA rather than less OA
26477312	In addition to the activation of oncogenes c-MYC and STAT3 in tumor cells, a number of cytokines and growth factors, such as IL1beta, IL6 and SPP1 (osteopontin, a key biomarker for PCa), were upregulated in NFATc1-induced PCa, establishing a tumorigenic microenvironment involving both NFATc1 positive and negative cells for prostate tumorigenesis
26460847	7 mul/ml boanmycin or bleomycin for 24 h and MTT was monitored from day 1 to day 9; senescence-associated beta-galactosidase staining, which indicated the cell senescence, was performed on day 7; and well-established senescence-associated secretory phenotype factor interleukin-6 expression was detected on day 9
26460847	Furthermore, quantitative PCR data also showed that the interleukin-6 expression was highly induced by boanmycin to six-fold in OBs
26433963	The search for mediators of senescent HPMC activity using specific neutralizing antibodies and recombinant exogenous proteins showed that the intensified angiogenic potential of cancer cells was elicited by IL-6 and TGF-beta1
26397719	In vitro treatment of primary human amnion epithelial cells with 40 muM T-oligos ([TTAGGG]2) that mimic telomere fragments, activated p38MAPK, produced senescence-associated (SA) beta-gal staining and increased interleukin (IL)-6 and IL-8 production compared to cells treated with complementary DNA sequences (Cont-oligos, [AATCCC]2)
26386121	We found that cigarette smoke accelerates telomere dysfunction via reactive oxygen species in vitro and may be associated with ataxia telangiectasia mutated-dependent secretion of inflammatory cytokines interleukin-6 and -8
26372907	Cellular senescence in four WAT depots was assessed using senescence-associated beta-galactosidase staining to quantify the senescent cell burden, and real-time qPCR to quantify gene expression of senescence markers p16 and IL-6
26284488	The search for mediators of senescent HPMC activity showed that increased SW480 cell proliferation was stimulated by IL-6, migration by CXCL8 and CCL2, invasion by IL-6, MMP-3 and uPA, and epithelial-mesenchymal transition by TGF-beta1
26240351	Concomitantly, increased cellular senescence in the adipose tissue from pol eta(-/-) mice was observed and measured by up-regulation of senescence markers, including p53, p16(Ink4a), p21, senescence-associated (SA) beta-gal activity, and SA secretion of proinflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) as early as 4 wk of age
26147250	Rapamycin reduced IL6 and other cytokine mRNA levels, but selectively suppressed translation of the membrane-bound cytokine IL1A
26147250	Reduced IL1A diminished NF-kappaB transcriptional activity, which controls much of the SASP; exogenous IL1A restored IL6 secretion to rapamycin-treated cells
26105007	Upon LPS treatment, SV cells also developed senescence-associated secretory phenotype (SASP), as demonstrated by the increased expression of TNFalpha, IL-1beta, IL-6, MCP-1, and VEGFalpha
26089914	For each early passage BM-MSC sample (5th or 6th passages), the normalized protein expression levels of senescence-associated markers p16(INK4A), p21(WAF1), SOD2, and rpS6(S240/244); the concentration of IL6 and IL8 in cell culture supernatants; and the normalized gene expression levels of pluripotency markers OCT4, NANOG, and SOX2 were correlated with final population doubling (PD) number
26025293	The concentration of proinflammatory SASP markers (granulocyte macrophage colony-stimulating factor, interleukin-6 and -8) was significantly higher in the amniotic fluid of women in labor at term than women not in labor
25989853	Functionally, impaired actin dynamics resulted in reduced NO secretion and reduced release of TNFalpha and IL-6 from LPS-stimulated microglia and of IGF-1 from IL-4 stimulated microglia
25972601	In these models, IL-6 and other cytokines were expressed mainly, if not exclusively, by the naturally occurring senescent cells (95
25972601	Furthermore, inhibition of IL-6 impaired the growth of the HER2-positive PDX (mean tumor volume at day 101, control vs anti-huIL-6 treated, 332
25964984	RESULTS: From baseline (day 0) to day 90, the activity of telomerase and levels of beta-endorphins, plasma cortisol, and interleukin-6 increased, and a sustained reduction in oxidative stress markers, such as reactive oxygen species and 8-hydroxy-2-deoxy-guanosine levels
25921542	Microarray analysis identified differentially regulated genes in response to LPC, which included the components of senescence-associated secretory phenotype (SASP) including interleukin-8 (IL-8), IL-6, transforming growth factor-beta and plasminogen activator inhibitor-1
25850282	The number of senescent cells was detected by SA-beta-Gal staining while the level of IL-1 and IL-6 proinflammatory cytokines in hippocampus were detected by ELISA
25850282	It is pointed that, in brain aging model group, the spatial learning and memory capacities were weaken, SA-beta-Gal positive granules increased in section of brain tissue, the activity of antioxidant enzyme SOD and the contents of GSH decreased in hippocampus, the level of IL-1 and IL-6 increased in hippocampus, while the length of telomere and the activity of telomerase decreased in hippocampus
25850282	Rats of Rg1 brain aging group had their spatial learning and memory capacities enhanced, SA-beta-Gal positive granules in section of brain tissue decreased, the activity of antioxidant enzyme SOD and the contents of GSH increased in hippocampus, the level of IL-1 and IL-6 in hippocampus decreased, the length contraction of telomere suppressed while the change of telomerase activity increased in hippocampus
25850282	Compared with that of normal group, the spatial learning and memory capacities were enhanced in Rg1 normal group, SA-beta-Gal positive granules in section of brain tissue decreased in Rg1 normal group, the level of IL-1 and IL-6 in hippocampus decreased in Rg1 normal group
25792544	In addition, the expression of cellular senescence features, such as the progressive rise in the enzymatic senescence-associated b-galactosidase (SA-b-gal) activity, IL6, IL1b, and TGFb expression, was observed throughout pituitary tumor development
25635860	The mRNAs and proteins of SASP components, such as IL-6 and IL-8, quickly accumulated in SIRT1-depleted cells, and the levels of these factors were also higher than those in control cells, indicating that SIRT1 negatively regulated the expression of SASP factors at the transcriptional level
25635860	SIRT1 bound to the promoter regions of IL-8 and IL-6, but dissociated from them during cellular senescence
25635860	The acetylation of Histone H3 (K9) and H4 (K16) of the IL-8 and IL-6 promoter regions gradually increased during cellular senescence
25635535	Silencing Arg-II or p38alpha in senescent cells recouples eNOS and inhibits IL-6 and IL-8 secretion
25604328	Immunosenescence was investigated by analysing CD57(+) CD28(-) levels, immune activation by analysing CD38(+) HLA-DR(+) levels, inflammation by analysing interleukin (IL)-6 levels, and microbial translocation by analysing lipopolysaccharide (LPS) and soluble CD14 (sCD14) levels
25604328	Also, levels of IL-6, LPS and especially sCD14, associated with bacterial translocation and additional monocyte activation, were significantly increased in patients with previous VL compared with patients with IDR (P = 0
25574956	Markers of T-cell activation and senescence were determined by flow cytometry, and plasma levels of interleukin-6, interleukin-8, and C-reactive protein (CRP) were measured, as was telomere length of peripheral blood mononuclear cells (PBMC)
25574956	RESULTS: Activated CD25(+) T cells and activated/senescent CD69(+)/CD57(+)/CD28(null) CD4(+) T cells, interleukin-6, and CRP were associated with PFT abnormalities
25572145	Another observation in the present study is the significant up-regulation of key senescence messaging factors regulated by NF-kappaB namely interleukin (IL)-6, IL-8, high-mobility group protein A (HMGA)1 and B (HMGB)1 in E2-transfected cells treated with TNF-alpha
25568096	Neuroglial cocultures displayed features of cellular senescence (increased senescence-associated-beta-galactosidase activity, oxidative stress, gamma-H2AX expression, IL-6 production, astrogliosis) that were concentration dependently counteracted by the antiaging compound resveratrol (1-5 microM)
25548483	The hepatocyte SASP included characteristic factors such as interleukin (IL)-8 and IL-6, as well as novel components such as SAA4, IL-32 and Fibrinogen, which were validated by qPCR and/or chemokine protein array
25536232	Furthermore, real-time polymerase chain reaction (PCR) showed that pretreatment with PS1145 inhibited the increase of mRNA expressions of interleukin-6 (IL-6) and p53-induced death domain (PIDD) protein, which have been show to play crucial roles in both senescence and apoptosis (P < 0
25512378	Oxidative stress-induced inhibition of Sirt1 by caveolin-1 promotes p53-dependent premature senescence and stimulates the secretion of interleukin 6 (IL-6)
25512378	Senescent cells secrete various growth factors and cytokines, such as IL-6, that can signal to the tumor microenvironment and promote cancer cell growth
25512378	We also identified IL-6 as a caveolin-1-specific cytokine that is secreted by senescent fibroblasts following the caveolin-1-mediated inhibition of Sirt1
25512378	The caveolin-1-mediated secretion of IL-6 by senescent fibroblasts stimulates the growth of cancer cells
25512378	Therefore, by inhibiting Sirt1, caveolin-1 links free radicals to the activation of the p53/senescence pathway and the protumorigenic properties of IL-6
25482089	Compared with normal pituitary cells, the aging pituitary tissues revealed increased expression of IL6, C/EBPbeta, p53, p21 and p16 and decreased expression of pituitary tumor transforming gene
25482089	In contrast, the expression of IL6, p21 and p16 was decreased in pituitary tumor cells compared with normal pituitary tissues
25482089	Taken together, multiple pathways including IL6/C/EBPbeta, p53/p21 and p16 were activated in aging pituitary cells in response to Dgal treatment
25419563	IL-6 secreted from senescent mesenchymal stem cells promotes proliferation and migration of breast cancer cells
25419563	In addition, we identified IL-6, a known pleiotropic cytokine, as a principal mediator for the tumor-promoting activity of s-UCMSCs by induction of STAT3 phosphorylation
25419563	Depletion of IL-6 from s-UCMSCs conditioned medium partially abrogated the stimulatory effect of s-UCMSCs on the proliferation and migration of breast tumor cells
25412309	We further demonstrate that PKCeta promotes senescence through its ability to upregulate the expression of the cell cycle inhibitors p21(Cip1) and p27(Kip1) and enhance transcription and secretion of interleukin-6 (IL-6)
25412309	Moreover, we demonstrate that PKCeta creates a positive loop for reinforcing senescence by increasing the transcription of both IL-6 and IL-6 receptor, whereas the expression of IL-8 is specifically suppressed by PKCeta
25412309	Furthermore, we show that the human polymorphic variant of PKCeta, 374I, that exhibits higher kinase activity in comparison to WT-374V, is also more effective in IL-6 secretion, p21(Cip1) expression and the promotion of senescence, further supporting a role for PKCeta in senescence
25385658	In addition, Abeta(1-42) upregulated interleukin (IL)-6 and IL-8 gene expression in the RPE-choroid
25364077	Senescence markers showed reduced TERT and cyclin A and increased p16INK4a expression, with higher IL-6 plasma levels in SF-exposed mice
25343365	3) with values for two anabolic hormones (serum dehydroepiandrosterone sulfate [DHEAS] and insulin growth factor [IGF]-1), four catabolic hormones (cortisol, epinephrine, norepinephrine, and interleukin-6 [IL-6]), and LTL were examined
25343365	We found that high IL-6 was associated with short LTL (
25319743	Stromovascular cell composition (flow cytometry), the number of senescent cells (senescence-associated-beta-galactosidase staining) and interleukin (IL)-6, IL-1, TNF-alpha and MCP1 mRNA (reverse transcription-PCR) were measured in each sample
25220188	Six genes independently correlated with either age (IL-6, TNFRSF-11B, IGFBP-3, SAA4, and COPG), prognosis (IL-6, SAA4), or the grade of the glioma (IL-6, IL-8, ICAM-1, IGFBP-3, and COPG)
25196711	Molecule activity was assessed on reactive oxygen species (ROS) production, on superoxide dismutase (SOD) and catalase activities and, finally, on inflammatory factor production IL-6, IL-8 and IL-1beta
25106938	Expression of senescence-associated genes p21, p16, and interleukin 6 (IL6) were also assessed
25046437	Interleukin-6 (IL-6) and IL-8 (protein and mRNA) were both increased compared with NHCs and H69s (all P<0
25040935	PIM-1 modulates cellular senescence and links IL-6 signaling to heterochromatin formation
25040935	Analysis of the mechanism underlying the up-regulation of PIM-1 expression during senescence demonstrated that IL-6, a critical regulator of cellular senescence, is responsible for PIM-1 induction
25040935	More importantly, we demonstrated that PIM-1 is also a direct target of IL-6/STAT3 signaling and mediates cytokine-induced cellular senescence
24979747	Further investigation showed that ginsenoside Rg1 protected NSCs/NPCs (neural stem cells/progenitor cells) shown by increased level of SOX-2 expression; reduced astrocytes activation shown by decrease level of Aeg-1 expression; increased the hippocampal cell proliferation; enhanced the activity of the antioxidant enzymes GSH-Px (glutathione peroxidase) and SOD (Superoxide Dismutase); decreased the levels of IL-1beta, IL-6 and TNF-alpha, which are the proinflammatory cytokines; increased the telomere lengths and telomerase activity; and down-regulated the mRNA expression of cellular senescence associated genes p53, p21Cip1/Waf1 and p19Arf in the hippocampus of aged rats
24828530	PKD1 is activated by oncogenic Ras expression and PKD1 promotes Ras OIS by mediating inflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8) via modulation of NF-kappaB activity
24828530	We demonstrate that ROS-protein kinase Cdelta (PKCdelta)-PKD1 axis is essential for the establishment and maintenance of IL-6/IL8 induction
24827852	Furthermore, quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) analysis revealed activation of the senescence-associated secretory phenotype (SASP), including the cytokines interleukin 6 (IL6) and 1alpha (IL1alpha)
24713392	We identify IL-6 as the mediator of M2-induced hepatocyte senescence
24665044	SASP markers, MMP-1/MMP-3 were significantly higher in the WSL but not IL-6/IL-8
24481487	The levels of circulatory inflammatory markers, including interleukin (IL) IL-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha) and interferon (INF-gamma), are known to increase associated to aging
24464501	Furthermore, levels of Il-6 increased in rats exposed to the carcinogenic protocol, while they returned to near control values in the group receiving hepatocyte transplantation
24439483	Inflammation markers (interleukin-6, c-reactive protein, tumor necrosis factor-alpha), hypothalamic-pituitary-adrenal-axis indicators (salivary cortisol awakening curve [area under the curve indicators, with respect to the ground and increase], evening levels, 0
24439483	Shorter LTL was significantly associated with higher c-reactive protein, interleukin-6, area under the curve with respect to increase, and heart rate
24416650	One such cytokine, interleukin-6 (IL-6), regulates senescence in some systems in addition to its known functions of immune regulation and promotion of tumorigenesis
24416650	In this review, we describe recent advances in studies on the roles of IL-6 and its downstream signal transducer and activator of transcription 3 (STAT3) in regulating premature cellular senescence
24416650	IL-6/sIL-6Ralpha stimulation forms a senescence-inducing circuit involving the STAT3-insulin-like growth factor-binding protein 5 (IGFBP5) as a key axis triggering and reinforcing component in human fibroblasts
24047696	Cellular senescence or EGFR signaling induces Interleukin 6 (IL-6) receptor expression controlled by mammalian target of rapamycin (mTOR)
24047696	Interleukin 6 (IL-6) signaling plays a role in inflammation, cancer, and senescence
24047696	Here, we identified soluble IL-6 receptor (sIL-6R) as a member of the senescence-associated secretory phenotype (SASP)
24047696	Moreover, aberrant EGF receptor (EGFR) activation triggered IL-6 synthesis
24047696	Our data suggest that mTOR serves as a central molecular switch to facilitate cellular IL-6 classic and trans-signaling via IL-6R upregulation with direct implications for cellular senescence and tumor development
24046862	We evaluated the effect on senescence by evaluating the senescence-associated proliferation arrest, the percentage of senescence-associated beta-galactosidase-positive cells, and the expression of senescent molecular markers such as IL-6 and MCP1
23953057	Although it is reported that interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3) is activated by human papillomavirus (HPV) infection in cervical cancer cells, little is known about the role of IL-6/STAT3 in tumour microenvironment during development of the disease
23953057	In this study, we found that cancer-associated fibroblasts (CAF) but not normal fibroblasts (NF) secrete high level of IL-6 with activated STAT3 and appear senescent at early passages in culture or in cervical cancer tissues infected with high-risk HPV, and that treatment of NF with recombinant IL-6 or CAF conditioned medium (CM) induces activation of STAT3 and cellular senescence
23953057	IL-6 and STAT3 are either upregulated or activated in Siha and Hela cells infected with HPV 16 or 18, but not in C33A and ME180 cells without HPV 16 or 18 infection
23953057	Overexpression of HPV early proteins 6 (E6) activates STAT3, increases IL-6 expression and tumour burden in C33A and ME180 cells, while silencing of HPV E6 by specific shRNA reduces STAT3 activation, IL-6 expression, and tumour formation in Siha and HeLa cells, so does silencing of STAT3 by specific shRNA in HeLa and C33A/E6 cells
23953057	The tumour growth of cervical cancer cells reconstituted with CAF or NF is largely affected by inhibition of fibroblast senescence with STAT3 inhibitor or with IL-6 antibody treatment
23953057	Thus, we have uncovered a mechanism that fibroblast senescence promotes cervical cancer development through high-risk HPV E6-activated IL-6/STAT3 signalling in tumour microenvironment
23952478	Morin significantly decreased the production of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in the UVB-irradiated KSC
23781024	Senescent cells secrete various growth factors and cytokines, such as IL6 and IL8, which collectively constitute the senescence-associated secretory phenotype (SASP)
23781024	RNAi-mediated knockdown of IkappaBzeta impaired IL6 and IL8 expression, whereas transgenic IkappaBzeta expression resulted in enhanced SASP cytokine expression
23742046	Aging also causes attenuation or alteration of many signalling pathways as well as the expression of transcription factors such as heat shock factor (HSF)
23727324	We previously reported that a biomarker combination including miR-146a, its target protein IL-1 receptor-associated kinase (IRAK-1), and released interleukin (IL)-6, here collectively designated as MIRAKIL, indicates senescence-associated secretory phenotype (SASP) acquisition by primary human umbilical vein endothelial cells (HUVECs)
23727324	However, short-term CoQ10H(2) supplementation attenuated LPS-induced MIRAKIL changes in young cells; in senescent cells CoQ10H(2) supplementation significantly attenuated LPS-induced miR-146a and IRAK-1 modulation but failed to curb IL-6 release
23719597	In primary PSC, doxorubicin treatment was associated with increased expression of interleukin-6 (IL-6) and matrix metalloproteinase (MMP)-9, while expression of the activation marker alpha-smooth muscle actin (alpha-SMA), p53, Cdk1 and Rad54 was diminished
23649808	Senescent cells also secrete inflammatory cytokines such as IL-6, which promote age-associated inflammation and pathology
23649808	HMGB1 depletion, HMGB1 blocking antibody, or TLR-4 inhibition attenuated senescence-associated IL-6 secretion, and exogenous HMGB1 stimulated NF-kappaB activity and restored IL-6 secretion to HMGB1-depleted cells
23644284	Transgenic Thy1-GFP rats and qRT-PCR demonstrated that failure of the regenerating axonal front in ANAs was associated with increased levels of senescence related markers in the graft (senescence associated beta-galactosidase, p16(INK4A), and IL6)
23591770	Radiation-induced senescence in securin-deficient cancer cells promotes cell invasion involving the IL-6/STAT3 and PDGF-BB/PDGFR pathways
23591770	The IL-6/STAT3 signalling loop and platelet-derived growth factor-BB (PDGF-BB)/PDGF receptor (PDGFR) pathway were important for CM-induced cell migration and invasion
23591770	Furthermore, CM promoted angiogenesis in the chicken chorioallantoic membrane though the induction of IL-6/STAT3- and PDGF-BB/PDGFR-dependent endothelial cell invasion
23583398	8-fold) and interleukin-6 (3
23385819	Adipocytes subjected to oxidative stress also showed shortened telomeres and increased mRNA and protein expression of p53, p21, TNF alpha and IL-6
23385065	Cellular senescence, a permanent state of cell cycle arrest that provides a barrier against tumorigenesis, is accompanied by elevated proinflammatory cytokines such as IL1, IL6, IL8 and TNFalpha
23385065	Whereas inhibition of IL6/STAT signaling had no effect on DDR induction in bystander cells, inhibition of either TGFbeta/SMAD or IL1/NFkappaB pathway resulted in decreased ROS production and reduced DDR in bystander cells
23375186	After adjustment for demographics, traditional risk factors, and inflammatory markers including high-sensitivity C-reactive protein, interleukin-6, and soluble intercellular adhesion molecule-1, those in the middle tertile had significantly elevated risk for incident CHD (hazard ratio 1
23296657	As an example, we discuss the assessment of the major SASP factor interleukin-6 in senescent human fibroblasts
23281008	This leads to enhanced secretion of inflammatory cytokines known to drive osteoclastogenesis, such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), and receptor activator of NF-kappaB ligand (RANKL), and thereby induces an inflammatory bone microenvironment favoring osteoclastogenesis
23117626	NF90 elicited these effects mainly by repressing the translation of target SASP mRNAs, since silencing NF90 did not increase the steady-state levels of SASP mRNAs but elevated key SASP factors including MCP-1, GROa, IL-6, and IL-8
23078884	Enforced Notch activation resulted in EC senescence and significantly upregulated expression of several molecules implicated in the inflammatory response (IL-6/IL-8/IL-1alpha/RANTES/ICAM-1)
23078884	The upregulated IL-6 was partially responsible for mediating leukocyte transendothelial migration
22904099	Compared with young EC, senescent cells displayed increased expression of senescence-associated beta-galactosidase, nitric oxide synthase (eNOS), and AKT kinase, and secreted increased amounts of growth factors (VEGF, TGF-beta), cytokines (IL-6, IL-8, MCP-1), adhesion molecules (sICAM-1), and matrix proteins (fibronectin)
22882466	About 40-80% of Purkinje neurons and 20-40% of cortical, hippocampal and peripheral neurons in the myenteric plexus from old C57Bl/6 mice showed severe DNA damage, activated p38MAPkinase, high ROS production and oxidative damage, interleukin IL-6 production, heterochromatinization and senescence-associated beta-galactosidase activity
22692848	2 % prevented tBHP-induced reactive oxygen species production (evaluated using the H2DCF-DA test in cytofluorometry) in epithelial cells and LPS-induced TNF-alpha and IL-6 release (evaluated using ELISA technique) in macrophages
22663935	We confirmed the importance of inflammatory markers (IL-6, TNF-alpha, CRP, neutrophils) in frailty in the very old, previously established only in younger-old populations
22452900	Senescent PSC highly expressed CDKN1A/p21, mdm2 and interleukin (IL)-6, but displayed low levels of alpha-smooth muscle actin
22404905	Suppression of the prototypical SASP component IL-6 required the glucocorticoid receptor, which, in the presence of ligand, inhibited IL-1alpha signaling and NF-kappaB transactivation activity
22404905	Accordingly, co-treatments combining glucocorticoids with the glucocorticoid antagonist RU-486 or recombinant IL-1alpha efficiently reestablished NF-kappaB transcriptional activity and IL-6 secretion
22392699	Furthermore, RS treatment increased levels of interleukin-6 in the liver, consistent with the activation of a senescence-associated secretory phenotype
22374671	The STAT3-IGFBP5 axis is critical for IL-6/gp130-induced premature senescence in human fibroblasts
22374671	One of these cytokines, interleukin-6 (IL6), not only functions in the immune system, but also promotes cellular senescence and cancer
22374671	Here we demonstrate that IL6 and the soluble IL6 receptor (sIL6R) induce premature senescence in normal human fibroblasts by establishing a senescence-inducing circuit involving the signal transducer and activator of transcription 3 (STAT3) and insulin-like growth factor-binding protein 5 (IGFBP5)
22374671	Stimulating TIG3 fibroblast cells with IL6/sIL6R sequentially caused an increase in reactive oxygen species (ROS) as early as day 1, followed by the DNA damage response, p53 accumulation and, finally, senescence on days 8-10
22374671	We found that STAT3 was required for the events leading to senescence, including the initial early-phase ROS increase and the induction of IL1alpha/beta, IL6 and CXCL8 mRNAs 4-5 d after IL6/sIL6R stimulation, suggesting that STAT3's role is indirect
22374671	We searched for STAT3-downstream molecule(s) responsible for the senescence-inducing activity in the supernatants of stimulated TIG3 and identified IGFBP5 as a major STAT3 mediator, because IGFBP5 was expressed from the early phase through the entire senescence process and was responsible for IL6/STAT3-induced ROS increase and premature senescence
22374671	Thus, IL6/sIL6R forms a senescence-inducing circuit involving the STAT3-IGFBP5 axis as a key triggering and reinforcing component
22362388	However, IL-6 and macrophage inflammatory protein 2 were increased in WT and cav-1(-/-) mice after bleomycin challenge, suggesting that bleomycin-induced inflammatory response substantiated the SASP pool
22358238	The expression levels of ELN, COL1A1, MMP1, CCND1, RB1, and IL6 genes were determined using the quantitative real-time polymerase chain reaction
22358238	CCND1, RB1, MMP1, and IL6 were upregulated in senescent fibroblasts
22319624	Both fatty acids appeared to abolish H(2)O(2) mediated stimulation of nuclear factor kappaB and IL-6, but not IL-1alpha and IL-8
22267761	The lung tissue in which type II cells contained higher numbers of gammaH2AX foci per cell had higher percentages of type II cells that expressed p16(INK4a) (p16), phosphorylated nuclear factor (NF)-kappaB and interleukin (IL)-6, and of alveolar wall cells that expressed active caspase-3
22267761	The type II cells that contained higher numbers of gammaH2AX foci per cell had higher rates of expression of p16, phosphorylated NF-kappaB, and IL-6
21680897	Telomere disruption increased monocyte secretion of monocyte chemoattractant protein-1, IL-6, and IL-1beta and oxidative burst, similar to that seen in coronary artery disease patients, and lymphocyte secretion of IL-2 and reduced lymphocyte IL-10
21602933	METHODOLOGY/PRINCIPAL FINDINGS: To address this issue, we examined if individuals with high levels of the systemic inflammatory markers interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein (CRP) had increased odds for short LTL
21602933	Logistic regression analyses indicated that individuals with high levels of either IL-6 or TNF-alpha had significantly higher odds for short LTL
21602933	Furthermore, individuals with high levels of both IL-6 and TNF-alpha had significantly higher odds for short LTL compared with those who had neither high (OR = 0
21602933	72), only IL-6 high (OR = 0
21602933	CONCLUSIONS/SIGNIFICANCE: Results suggest that cumulative inflammatory load, as indexed by the combination of high levels of IL-6 and TNF-alpha, is associated with increased odds for short LTL
21536657	CPEB knockout mouse embryo fibroblasts (MEFs) bypass senescence and synthesize large amounts of interleukin-6 (IL-6) and many other cytokines, which is not the case with either wild-type MEFs immortalized by prolonged culture or p53-deficient MEFs
21536657	CPEB regulates the production of IL-6 at both the translational and transcriptional levels; in CPEB-depleted cells, aberrant IL-6 transcription is mediated by improper NF-kappaB p65 phosphorylation and nuclear localization
21536657	Although IL-6 strengthens the senescence of wild-type cells, it has no effect on CPEB-deficient cells, even though they produce prodigious amounts of the cytokine
21536657	IL-6-promoted entry into senescence requires p53; CPEB knockout MEFs, however, synthesize only approximately 50% of the p53 of wild-type MEFs, which is insufficient to respond to IL-6
21536657	Thus, CPEB deficiency not only increases IL-6 production but also renders the cell incapable of a senescence-promoting response
21448457	METHODOLOGY: Leukocyte telomere length was compared between 18 unmedicated MDD subjects and 17 controls and was correlated with lifetime depression chronicity and peripheral markers of oxidation (F2-isoprostane/Vitamin C ratio) and inflammation (IL-6)
21336305	We demonstrate that retinoic-acid-inducible gene-I (RIG-I) is induced through the ataxia telangiectasia mutated-interferon regulatory factor 1 (ATM-IRF1) axis in senescent cells and that RIG-I signalling mediates the expression of two important mediators of inflammation, interleukin-6 (IL-6) and IL-8
21336305	We show here that the intracellular, but not the secreted, form of klotho interacts with RIG-I and that this interaction inhibits RIG-I-induced expression of IL-6 and IL-8 both in vitro and in vivo
21148804	14), including 58 dementia family caregivers and 74 non-caregivers, blood samples were analyzed for interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and telomere length, a measure of cell aging
21148804	RESULTS: After controlling for age, caregiving status, gender, body mass index, exercise, and sleep, the presence of multiple childhood adversities was related to both heightened IL-6 (0
21148804	Abuse was associated with heightened IL-6 and TNF-alpha levels; for TNF-alpha, this relationship was magnified in caregivers compared with controls
21084274	Many of these induced mRNA changes are in secreted proteins, IL-6, IL-8, and IL-11 and chemokines CXCL2 and CXCL5, or genes associated with an "inflammatory" phenotype
21084274	Evidence indicates that the induction of senescence occurs as a result of reactive oxygen species elevation followed by low-level activation of the caspase cascade, insufficient to induce apoptosis, but sufficient to lead to minor DNA damage and increases in p53, p21, IL-6 and 8 proteins
21047732	In DAOY cells, senescence-associated secretory factors, such as interleukin-6 and insulin-like growth factor binding protein 7, were strongly upregulated after OTX2 induction
20861074	Both INK4a knockout mesangial cells and kidney lysates from knockout mice following injury showed elevated levels of IL-6 by ELISA compared with WT samples
20647331	In 22Rv1 human prostate cells, but not in Du145 or RWPE-2, PIM1 overexpression was associated with marked increases in cellular senescence, as shown by changes in the levels of beta-galactosidase (SA-beta-Gal), p21, interleukin (IL)-6 and IL-8 mRNA and protein
20053980	Protein levels of IRAK1 and PAI-1 were analyzed by Western blot and those of IL6 and IL8 by ELISA
20016134	RESULTS: Senescent A549 cells and HDMECs, whether stimulated with lipopolysaccharide or not, produced greater amounts of IL-6, IL-8 and TNF-alpha, which paralleled NF-kappaB activation, than did presenescent cells
20006787	Chronic inflammation, characterized by increased serum levels of tumor necrosis factor-alpha, interleukin-6, C-reactive protein, and plasminogen activator inhibitor-1, and the presence of inflammatory-related diseases, are seen commonly in aging
19935801	In addition, these cells secrete higher levels of IL-6 and IL-8 representing key components of the senescence-associated secretory phenotype (SASP) with the ability to impact on neighbouring cells
19805069	Cell surface-bound IL-1alpha is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network
19805069	We show that cell surface-bound IL-1alpha is essential for signaling the senescence-associated secretion of IL-6 and IL-8, 2 proinflammatory cytokines that also reinforce the senescence growth arrest
19805069	An IL-1 receptor (IL1R) antagonist, neutralizing IL-1alpha antibodies, and IL-1alpha depletion by RNA interference all markedly reduced senescence-associated IL-6/IL-8 secretion
19805069	Furthermore, IL-1alpha depletion reduced the DNA binding activity of NF-kappaB and C/EBPbeta, which stimulate IL-6/IL-8 transcription
19805069	IL-1alpha was a general regulator of senescence-associated IL-6/IL-8 secretion because IL-1alpha blockade reduced IL-6/IL-8 secretion whether cells senesced owing to DNA damage, replicative exhaustion, oncogenic RAS, or chromatin relaxation
19805069	Furthermore, conditioned medium from IL-1alpha-depleted senescent cells markedly reduced the IL-6/IL-8-dependent invasiveness of metastatic cancer cells, indicating that IL-1alpha regulates the biological effects of these cytokines
19805069	Thus, cell surface IL-1alpha is an essential cell-autonomous regulator of the senescence-associated IL-6/IL-8 cytokine network
19802007	JAK1/STAT-activating ligands, interleukin 10 (IL10), IL20, IL24, interferon gamma (IFNgamma), IFNbeta and IL6, were also expressed by senescent cells, supporting autocrine/paracrine activation of JAK1/STAT
19730126	Postinfarct cardiac remodeling was associated with increased atrial natriuretic peptide, interleukin-6 and connective tissue growth factor mRNA expressions, as well as three-fold increased cardiomyocyte senescence, measured as cardiac p16 mRNA expression
19730126	Levosimendan also ameliorated MI-induced atrial natriuretic peptide, IL-6, and connective tissue growth factor overexpression as well as MI-induced disturbances in calcium-handling proteins (SERCA2, Na-Ca exchanger) without changes in diabetic status or systemic blood pressure
19650831	This characteristic phenotype included persistently activated DNA damage signalling (detected as 53BP1/gammaH2AX(+) foci), enhanced senescence-associated beta-galactosidase activity, expansion of promyelocytic leukaemia nuclear compartments and induced expression of several cytokines (especially interleukins IL-6, IL-8 and IL-24), overall features shared by cells undergoing replicative or premature cellular senescence
19597488	We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs), which initiate increased secretion of inflammatory cytokines such as interleukin-6 (IL-6)
19597488	ATM was also essential for IL-6 secretion during oncogene-induced senescence and by damaged cells that bypass senescence
19597488	Furthermore, DDR activity and IL-6 were elevated in human cancers, and ATM-depletion suppressed the ability of senescent cells to stimulate IL-6-dependent cancer cell invasiveness
19584087	We have identified a significantly altered cellular phenotype in response to chronic hypoxia as characterized by increased receptor-mediated apoptotic resistance, the induction of cellular senescence, increased invasion and the increased secretion of IL-1 beta, IL6, IL8 and TNFalpha cytokines
19572808	However, FA MSCs showed reduced long-term proliferation ability, higher stem cell factor and interleukin-6 levels, and increased expression of senescent-associated beta-galactosidase compared to normal MSCs, suggesting a potential role of the BM microenvironment in long-term BMF
19526322	The mRNA levels of IL6, as well as its secretion, increased as preadipocytes matured and became old cells; a similar trend was also found for MCP-1
19526322	LPS significantly increased the mRNA levels of IL-6, as well as its secretion, with a similar trend also observed for MCP-1
19325234	IL-6 and IL-8, two well-known proinflammatory cytokines, seem to play a central role in premature cellular senescence induction
19053174	In cultured premalignant epithelial cells, SASPs induced an epithelial-mesenchyme transition and invasiveness, hallmarks of malignancy, by a paracrine mechanism that depended largely on the SASP factors interleukin (IL)-6 and IL-8
19027816	Resveratrol treatment effectively prevented increased production of intracellular reactive oxygen species (iROS) and inflammatory markers (IL1alpha, IL6, IL8, and ELAM-1), and reduced expression of the senescence markers sa-beta-gal, lipofuscin, and accumulation of carbonylated proteins
18838863	Importantly, our data adds to that presented by several groups suggesting that also other factors secreted during senescence (such as PAI-1, IGFBP-7 or IL-6) contribute to the senescent response
18555778	Induced genes included the pleiotropic cytokine interleukin-6 (IL-6), which upon secretion by senescent cells acted mitogenically in a paracrine fashion
18555778	Unexpectedly, IL-6 was also required for the execution of OIS, but in a cell-autonomous mode
18555778	Furthermore, we demonstrate that the transcription factor C/EBPbeta cooperates with IL-6 to amplify the activation of the inflammatory network, including IL-8
18206730	CD34+ cells were expanded for 3 weeks with stem cell factor, Flt-3/Flk-2 ligand, thrombopoietin, and interleukin-6
17785060	OBJECTIVE: To investigate the effects of epigallocatechin-3-gallate (EGCG) on the cell aging and hypoxanthine-phosphoribosyl-transferase (HPRT) gene mutation frequency induced by long-term ultraviolet (UV) A and UVB irradiation in human skin fibroblasts (HSF)
17785060	METHODS: HSF were separated from infant foreskin, cultured, and divided into six groups: control, EGCG group (treated by 25 microg/ml EGCG), UVA group (irradiated by 10 J/cm(2) UVA for 2 weeks), UVB group (irradiated by 30 mJ/cm(2) UVB for 2 weeks), UVA + EGCG group and UVB + EGCG group
16543712	Although higher in HD group, inflammatory indexes (C-reactive protein, interleukin-6, IL-6, soluble IL-6 and soluble gp130) were not correlated to telomerase activity in PBMCs
16336976	Interleukin-6 (IL-6) is an autocrine promoter of cholangiocarcinoma growth
16336976	IL-6 increased telomerase activity and decreased cellular senescence during repeated passaging
16336976	CONCLUSION: Enhanced telomerase activity in response to IL-6 stimulation can prevent cellular senescence and thereby contribute to cholangiocarcinoma growth
15970415	Immediately after heat stress, or 24 h later, the myocardium was examined for either activation of the heat shock transcription factor (HSF) or HSP 72 accumulation
15970415	Hearts from heat stressed CR animals demonstrated an increased HSF activation and an increased HSP 72 content when compared to hearts from heat stressed aged animals
15970415	The HSF response and HSP 72 content of the hearts from heat stressed aged CR animals was comparable to that observed in hearts from heat stressed adult animals
15685514	Expression of p53, CD14/CD16, and intracellular cytokine production (interleukin-1beta [IL-1beta], IL-6, and IL-4) was evaluated by means of flow cytometry using specific antibodies
15685514	RESULTS: Features of senescence were found in a subpopulation of mononuclear cells: (1) accelerated telomere shortening, (2) increased p53 expression, (3) CD14dim/CD16bright expression, and (4) cytokine overproduction (IL-1beta, IL-6, and IL-4)
15685514	Finally, mononuclear cells from hemodialysis patients, but not controls, spontaneously produced the proinflammatory cytokines IL-1beta and IL-6
15037008	Another useful biomarker of cellular aging in the monkey is interleukin-6 (IL-6) release
15037008	For example, when endothelial cell cultures were generated from cerebral blood vessels, those derived from aged donors produced significantly more IL-6 in response to IL-1, LPS, and hypoxia
12784623	Fully senescent A549 cells were elongated, acquired contact inhibition capabilities when reaching confluence, and secreted the senescence-associated cytokine IL-6
10867642	In contrast to the rapid heat shock transcription factor (HSF) activation, apoptosis occurred only after long-term exposure to hypo-osmotic or hyperosmotic stress
10439372	To better understand regulatory mechanisms of telomerase, in relationship with apoptosis and the cell cycle, we examined telomerase activity in PCM6, an interleukin-6 (IL-6)-responsive, interferon-alpha (IFN-alpha)-sensitive multiple myeloma cell line, using a PCR-based assay
9722719	Amounts of PGE2, interleukin (IL)-1 beta, IL-6, and plasminogen activator (PA) in conditioned media were measured
9722719	LPS-stimulated PGE2, IL-1 beta, IL-6, and PA production was increased in "old" HGF compared to younger cells
9722719	According to RT-PCR analysis, gene expression of COX-2, IL-1 beta, IL-6, and tissue type (t) PA was higher in old cells than in young cells
9680181	The activation of NF-kappaB has been recognized to regulate a number of genes necessary for normal T cell responses including IL-2, IL-6, IL-8, and several T cell surface receptors
9190953	Although there was no significant difference in steady-state serum amyloid A level in the serum of aged non-Tg and Fas-Tg mice, challenging mice with staphylococcal enterotoxin B resulted in significantly higher serum levels of serum amyloid A on day 2 and IL-6 on days 1 and 2 and a higher magnitude of weight loss on day 7 in aged Fas-Tg mice compared with young mice
8735906	In vitro senescence enhances IL-6 production in human gingival fibroblasts induced by lipopolysaccharide from Campylobacter rectus
8735906	The production of interleukin-6 (IL-6) in human gingival fibroblasts (Gin cells) is increased by lipopolysaccharide (LPS) from Campylobacter rectus (C
8735906	Levels of IL-6 released in the medium were measured after incubation for 3, 6, 9, 12, and 24 h
8735906	Using cells from each of the three donors, we found that this phenomenon of higher LPS-stimulated IL-6 production in senescent cells was reproducible
8735906	The greater capacity of the senescent cells to synthesize IL-6 in response to LPS was a higher production of mRNA for IL-6
8735906	This increase of IL-6 production induced by C
7737374	On exposure to TNF, senescent HDF produced IL-6 and IL-8, but to a much lower degree than that produced by young HDF
8034686	Basal and induced amounts of interleukin-6 mRNA decline progressively with age in human fibroblasts
8034686	Interleukin-6 (IL-6) is a multi-functional cytokine that plays a role in the body's response to injury and infection
8034686	IL-6 expression is induced in young human diploid fibroblasts (HDF) in response to a number of agents including fetal bovine serum, 12-O-tetradecanoylphorbol-13-acetate, double-stranded RNA, and forskolin
8034686	In contrast, we find that senescent HDF are markedly deficient in their ability to express IL-6 in response to serum, double-stranded RNA, and 12-O-tetradecanoyl-phorbol-13-acetate, whereas forskolin is still an effective inducer for senescent cells
8034686	Thus, specific pathways for stimulating IL-6 expression appear to be blocked in senescent HDF
8034686	The basal amount of IL-6 mRNA in unstimulated senescent HDF is also much lower than in unstimulated young quiescent HDF
8034686	Likewise, the amount of IL-6 protein produced by senescent HDF is decreased at least 10-fold
8034686	Both the basal and induced levels of IL-6 declined progressively with aging of the HDF in culture, e
8034686	IL-6 cannot be induced above the young basal level by approximately 65% of life-span completed
8034686	If a similar decrease in IL-6 expression takes place in HDF in vivo, it could contribute to the decline in wound healing and the increase in the number and severity of infections experienced by aged individuals
8262134	This occurred despite the TNF-dependent induction of such proliferation-independent genes as manganese superoxide dismutase and interleukin-6 in senescent and quiescent cells
6946268	Prostaglandin production is also related to senescence in human skin fibroblasts (HSF)
6946268	Prostacyclin production in response to bradykinin drops in HSF as they are obtained from individuals of increasing chronologic age

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HCSGD entry for IL6

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Gene occurances in abstracts of cellular senescence-associated articles: 143 abstracts the gene occurs.

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