HCSGD entry for TNF
1. General information
| Official gene symbol | TNF |
|---|---|
| Entrez ID | 7124 |
| Gene full name | tumor necrosis factor |
| Other gene symbols | DIF TNF-alpha TNFA TNFSF2 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000060 | Protein import into nucleus, translocation | IDA | biological_process |
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IDA | biological_process |
| GO:0000165 | MAPK cascade | IMP | biological_process |
| GO:0000185 | Activation of MAPKKK activity | IDA | biological_process |
| GO:0000187 | Activation of MAPK activity | IDA | biological_process |
| GO:0001666 | Response to hypoxia | IEA | biological_process |
| GO:0001775 | Cell activation | IEA | biological_process |
| GO:0001819 | Positive regulation of cytokine production | IDA | biological_process |
| GO:0001891 | Phagocytic cup | ISS | cellular_component |
| GO:0001934 | Positive regulation of protein phosphorylation | IDA | biological_process |
| GO:0002020 | Protease binding | IPI | molecular_function |
| GO:0002037 | Negative regulation of L-glutamate transport | IEA | biological_process |
| GO:0002439 | Chronic inflammatory response to antigenic stimulus | IMP | biological_process |
| GO:0002740 | Negative regulation of cytokine secretion involved in immune response | IDA | biological_process |
| GO:0002876 | Positive regulation of chronic inflammatory response to antigenic stimulus | IEA | biological_process |
| GO:0002925 | Positive regulation of humoral immune response mediated by circulating immunoglobulin | IEA | biological_process |
| GO:0003009 | Skeletal muscle contraction | IEA | biological_process |
| GO:0005125 | Cytokine activity | IDA | molecular_function |
| GO:0005164 | Tumor necrosis factor receptor binding | IDA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005576 | Extracellular region | TAS | cellular_component |
| GO:0005615 | Extracellular space | IDA | cellular_component |
| GO:0005886 | Plasma membrane | TAS | cellular_component |
| GO:0005887 | Integral component of plasma membrane | IDA | cellular_component |
| GO:0006006 | Glucose metabolic process | IEA | biological_process |
| GO:0006915 | Apoptotic process | TAS | biological_process |
| GO:0006919 | Activation of cysteine-type endopeptidase activity involved in apoptotic process | IDA | biological_process |
| GO:0006927 | Transformed cell apoptotic process | IDA | biological_process |
| GO:0006954 | Inflammatory response | IDA | biological_process |
| GO:0006959 | Humoral immune response | IEA | biological_process |
| GO:0007254 | JNK cascade | IEA | biological_process |
| GO:0008285 | Negative regulation of cell proliferation | IEA | biological_process |
| GO:0008625 | Extrinsic apoptotic signaling pathway via death domain receptors | IDA NAS | biological_process |
| GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | IEA | biological_process |
| GO:0008652 | Cellular amino acid biosynthetic process | IEA | biological_process |
| GO:0009612 | Response to mechanical stimulus | IEA | biological_process |
| GO:0009615 | Response to virus | IDA | biological_process |
| GO:0009651 | Response to salt stress | TAS | biological_process |
| GO:0009887 | Organ morphogenesis | IEA | biological_process |
| GO:0009897 | External side of plasma membrane | ISS | cellular_component |
| GO:0009986 | Cell surface | IDA | cellular_component |
| GO:0010629 | Negative regulation of gene expression | IDA | biological_process |
| GO:0010693 | Negative regulation of alkaline phosphatase activity | IEA | biological_process |
| GO:0010888 | Negative regulation of lipid storage | NAS | biological_process |
| GO:0010940 | Positive regulation of necrotic cell death | TAS | biological_process |
| GO:0014823 | Response to activity | IEA | biological_process |
| GO:0019722 | Calcium-mediated signaling | IEA | biological_process |
| GO:0030198 | Extracellular matrix organization | IEA | biological_process |
| GO:0030316 | Osteoclast differentiation | IEA | biological_process |
| GO:0030730 | Sequestering of triglyceride | IDA | biological_process |
| GO:0031334 | Positive regulation of protein complex assembly | IDA | biological_process |
| GO:0031622 | Positive regulation of fever generation | ISS | biological_process |
| GO:0031663 | Lipopolysaccharide-mediated signaling pathway | IDA | biological_process |
| GO:0032715 | Negative regulation of interleukin-6 production | IDA | biological_process |
| GO:0032722 | Positive regulation of chemokine production | IDA | biological_process |
| GO:0032729 | Positive regulation of interferon-gamma production | IEA | biological_process |
| GO:0032741 | Positive regulation of interleukin-18 production | IEA | biological_process |
| GO:0032755 | Positive regulation of interleukin-6 production | IEA | biological_process |
| GO:0032800 | Receptor biosynthetic process | IDA | biological_process |
| GO:0033138 | Positive regulation of peptidyl-serine phosphorylation | IDA | biological_process |
| GO:0033209 | Tumor necrosis factor-mediated signaling pathway | IMP | biological_process |
| GO:0034116 | Positive regulation of heterotypic cell-cell adhesion | IDA | biological_process |
| GO:0042346 | Positive regulation of NF-kappaB import into nucleus | IDA | biological_process |
| GO:0042493 | Response to drug | IEA | biological_process |
| GO:0042802 | Identical protein binding | IDA | molecular_function |
| GO:0043065 | Positive regulation of apoptotic process | IDA | biological_process |
| GO:0043068 | Positive regulation of programmed cell death | IDA | biological_process |
| GO:0043122 | Regulation of I-kappaB kinase/NF-kappaB signaling | IDA | biological_process |
| GO:0043123 | Positive regulation of I-kappaB kinase/NF-kappaB signaling | IDA | biological_process |
| GO:0043242 | Negative regulation of protein complex disassembly | IDA | biological_process |
| GO:0043243 | Positive regulation of protein complex disassembly | IDA | biological_process |
| GO:0043280 | Positive regulation of cysteine-type endopeptidase activity involved in apoptotic process | IDA | biological_process |
| GO:0043406 | Positive regulation of MAP kinase activity | IDA | biological_process |
| GO:0043491 | Protein kinase B signaling | IMP | biological_process |
| GO:0043507 | Positive regulation of JUN kinase activity | IDA | biological_process |
| GO:0043525 | Positive regulation of neuron apoptotic process | IEA | biological_process |
| GO:0044130 | Negative regulation of growth of symbiont in host | IEA | biological_process |
| GO:0044212 | Transcription regulatory region DNA binding | IDA | molecular_function |
| GO:0045071 | Negative regulation of viral genome replication | IDA | biological_process |
| GO:0045080 | Positive regulation of chemokine biosynthetic process | IDA | biological_process |
| GO:0045121 | Membrane raft | IDA | cellular_component |
| GO:0045416 | Positive regulation of interleukin-8 biosynthetic process | IDA | biological_process |
| GO:0045429 | Positive regulation of nitric oxide biosynthetic process | IDA | biological_process |
| GO:0045599 | Negative regulation of fat cell differentiation | NAS | biological_process |
| GO:0045668 | Negative regulation of osteoblast differentiation | IEA | biological_process |
| GO:0045672 | Positive regulation of osteoclast differentiation | IDA | biological_process |
| GO:0045840 | Positive regulation of mitosis | IEA | biological_process |
| GO:0045892 | Negative regulation of transcription, DNA-templated | IDA | 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 IGI | biological_process |
| GO:0045994 | Positive regulation of translational initiation by iron | IEA | biological_process |
| GO:0046325 | Negative regulation of glucose import | IEA | biological_process |
| GO:0046330 | Positive regulation of JNK cascade | IEA | biological_process |
| GO:0048566 | Embryonic digestive tract development | IEP | biological_process |
| GO:0048661 | Positive regulation of smooth muscle cell proliferation | IDA | biological_process |
| GO:0050715 | Positive regulation of cytokine secretion | IDA | biological_process |
| GO:0050796 | Regulation of insulin secretion | IDA | biological_process |
| GO:0050806 | Positive regulation of synaptic transmission | IEA | biological_process |
| GO:0050830 | Defense response to Gram-positive bacterium | IEA | biological_process |
| GO:0050901 | Leukocyte tethering or rolling | IDA | biological_process |
| GO:0050995 | Negative regulation of lipid catabolic process | IDA | biological_process |
| GO:0051023 | Regulation of immunoglobulin secretion | IEA | biological_process |
| GO:0051044 | Positive regulation of membrane protein ectodomain proteolysis | 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:0051222 | Positive regulation of protein transport | IDA | biological_process |
| GO:0051384 | Response to glucocorticoid | IDA | biological_process |
| GO:0051533 | Positive regulation of NFAT protein import into nucleus | IDA | biological_process |
| GO:0051798 | Positive regulation of hair follicle development | IEA | biological_process |
| GO:0051897 | Positive regulation of protein kinase B signaling | IEA | biological_process |
| GO:0055037 | Recycling endosome | ISS | cellular_component |
| GO:0060557 | Positive regulation of vitamin D biosynthetic process | IDA | biological_process |
| GO:0060559 | Positive regulation of calcidiol 1-monooxygenase activity | IDA | biological_process |
| GO:0060664 | Epithelial cell proliferation involved in salivary gland morphogenesis | IEA | biological_process |
| GO:0060693 | Regulation of branching involved in salivary gland morphogenesis | IEA | biological_process |
| GO:0061048 | Negative regulation of branching involved in lung morphogenesis | IDA | biological_process |
| GO:0070265 | Necrotic cell death | IDA | biological_process |
| GO:0070374 | Positive regulation of ERK1 and ERK2 cascade | NAS | biological_process |
| GO:0071230 | Cellular response to amino acid stimulus | IEA | biological_process |
| GO:0071316 | Cellular response to nicotine | IDA | biological_process |
| GO:0071407 | Cellular response to organic cyclic compound | IDA | biological_process |
| GO:0071677 | Positive regulation of mononuclear cell migration | NAS | biological_process |
| GO:0071803 | Positive regulation of podosome assembly | IDA | biological_process |
| GO:0097190 | Apoptotic signaling pathway | TAS | biological_process |
| GO:0097191 | Extrinsic apoptotic signaling pathway | IDA | biological_process |
| GO:0097527 | Necroptotic signaling pathway | IDA | biological_process |
| GO:1902043 | Positive regulation of extrinsic apoptotic signaling pathway via death domain receptors | IEA | biological_process |
| GO:2000010 | Positive regulation of protein localization to cell surface | IDA | biological_process |
| GO:2000343 | Positive regulation of chemokine (C-X-C motif) ligand 2 production | IDA | biological_process |
| GO:2001240 | Negative regulation of extrinsic apoptotic signaling pathway in absence of ligand | IDA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.5440434102 | 0.8812284488 | 0.9999902473 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Up | 0.0194788988 |
| GSE13712_SHEAR | Up | 0.1344824462 |
| GSE13712_STATIC | Down | -0.0903697046 |
| GSE19018 | Up | 0.1231898768 |
| GSE19899_A1 | Down | -0.0058511665 |
| GSE19899_A2 | Down | -0.3686982128 |
| PubMed_21979375_A1 | Down | -0.0906462953 |
| PubMed_21979375_A2 | Down | -0.0858993620 |
| GSE35957 | Up | 0.0860493550 |
| GSE36640 | Up | 0.0994947636 |
| GSE54402 | Up | 0.0457163384 |
| GSE9593 | Up | 0.1265056758 |
| GSE43922 | Up | 0.0674889738 |
| GSE24585 | Up | 0.2546662673 |
| GSE37065 | Up | 0.0250861875 |
| GSE28863_A1 | Down | -0.0004431785 |
| GSE28863_A2 | Up | 0.1431519688 |
| GSE28863_A3 | Up | 0.0541690061 |
| GSE28863_A4 | Up | 0.1280788192 |
| GSE48662 | Up | 0.0224178188 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Etanercept | DB00005 | BTD00052 | BIOD00052 |
| Adalimumab | DB00051 | BTD00049 | BIOD00049 |
| Infliximab | DB00065 | BTD00004 | BIOD00004 |
| Chloroquine | DB00608 | APRD00468 |
| Glucosamine | DB01296 | EXPT01563 |
| Pranlukast | DB01411 | - |
| Amrinone | DB01427 | - |
| Isopropyl Alcohol | DB02325 | EXPT01912 | DB04402 |
| Afelimomab | DB04956 | - |
| YSIL6 | DB05017 | - |
| AV411 | DB05066 | - |
| SD118 | DB05207 | - |
| PN0621 | DB05218 | - |
| 681323 | DB05250 | - |
| OMS-103HP | DB05303 | - |
| SCIO-469 | DB05412 | - |
| VX-702 | DB05470 | - |
| Apremilast | DB05676 | - |
| CRx-139 | DB05744 | - |
| CYT007-TNFQb | DB05758 | - |
| HMPL-004 | DB05767 | - |
| CTI-01 | DB05869 | - |
| AME-527 | DB05879 | - |
| Golimumab | DB06674 | - |
| Certolizumab pegol | DB08904 | - |
| Pomalidomide | DB08910 | - |
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-203a | MIMAT0000264 | MIRT006857 | Luciferase reporter assay | Functional MTI | 22917968 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-19a-3p | MIMAT0000073 | 1 | hsa-miR-19a | {Western blot} | {downregulation by anti-miRNA oligonucleotide} | 21271217 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 81 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 |
| 27547293 | Compared to their normobilirubinemic siblings, aged hyperbilirubinemic Gunn rats showed significantly smaller amounts of visceral fat, better glucose tolerance, and decreased serum levels of proinflammatory cytokines TNFalpha, IL-1beta, and IL-18 |
| 27147278 | Prominent examples include aberrations in cytokines and their signaling pathways (such as tumor necrosis factor-alpha, interferon-gamma, SMAD proteins), mutations in genes encoding the RNA splicing machinery (SF3B1, SRSF2, ZRSR2, and U2AF1 genes), mutations in genes disrupting the epigenetic machinery (TET2, DNMT3A, DNMT3B, EZH2, ASXL1) |
| 27076598 | Endogenous Transmembrane TNF-Alpha Protects Against Premature Senescence in Endothelial Colony Forming Cells |
| 27076598 | RATIONALE: Transmembrane tumor necrosis factor-alpha (tmTNF-alpha) is the prime ligand for TNF receptor 2, which has been shown to mediate angiogenic and blood vessel repair activities in mice |
| 27076598 | Indeed, the mechanism of chronic inflammation-induced premature senescence involves an abrogation of tmTNF/TNF receptor 2 signaling |
| 26943583 | Aim of this study was to evaluate whether and how adalimumab, a monoclonal antibody directed against tumor necrosis factor-alpha (TNF-alpha), a major SASP component, can prevent the SASP |
| 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 |
| 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 |
| 26522327 | By contrast, inflammatory stimuli such as lipopolysaccharide (LPS) and tumor necrosis factor-alpha promoted HMGB1 release by provoking its dissociation from SIRT1 dependent on acetylation, thereby increasing the association between HMGB1 and chromosome region maintenance 1, leading to HMGB1 translocation |
| 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) |
| 26388614 | Disc in flames: Roles of TNF-alpha and IL-1beta in intervertebral disc degeneration |
| 26388614 | Inflammatory processes exacerbated by cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) are believed to be key mediators of disc degeneration and low back pain |
| 26388614 | In this review, we describe the contributions of TNF-alpha and IL-1beta to changes seen during disc degeneration at both cellular and tissue level, as well as new evidence suggesting a link between infection of the spine and low back pain, and the emerging therapeutic modalities aimed at combating these processes |
| 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 |
| 26142204 | Vasodilator responses to acetylcholine (Ach) in the isolated aortic rings were measured, serum concentration of glucose, tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) and the expression of VPO1 in the aorta were determined |
| 26142204 | Endothelial cells were treated with high glucose or H2O2, the concentrations of MCP-1, TNF-alpha and hypochlorous acid (HOCl) and the expression of VPO1 were determined |
| 26142204 | RESULTS: Vasodilator responses to Ach were impaired markedly and the serum concentrations of glucose, TNF-alpha and MCP-1 were significantly increased in diabetic rats |
| 26142204 | High glucose treatment significantly decreased cell viability and elevated the levels of MCP-1, TNF-alpha and HOCl and upregulated the expression of VPO1 |
| 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 |
| 26091153 | In vitro data suggested a mechanism implicating a role of TNF-alpha and IL-1beta in disc autophagy |
| 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 |
| 25982278 | While cytokines such as tumor necrosis factor-alpha (TNFalpha) and interferon gamma (IFNgamma) are important components of senescence-associated secretome and induce senescence in, for example, mouse pancreatic beta-cancer cell model, their downstream signaling pathway(s) and links with oxidative stress and DDR are mechanistically unclear |
| 25982278 | Using human and mouse normal and cancer cell models, we now show that TNFalpha and IFNgamma induce NADPH oxidases Nox4 and Nox1, reactive oxygen species (ROS), DDR signaling and premature senescence |
| 25982278 | Unlike mouse tumor cells that required concomitant presence of IFNgamma and TNFalpha, short exposure to IFNgamma alone was sufficient to induce Nox4, Nox1 and DDR in human cells |
| 25894557 | The penises injected with the senescent cells expressed human IL-1beta and subsequently endogenous proinflammatory cytokines such as mouse IL-1beta and tumor necrosis factor-alpha |
| 25572145 | Re-expression of HPV16 E2 in SiHa (human cervical cancer) cells potentiates NF-kappaB activation induced by TNF-alpha concurrently increasing senescence and survival |
| 25572145 | Re-expression of E2 expression with TNF-alpha treatment resulted in an increase in the expression of anti-apoptotic Bcl2 (B-cell lymphoma 2) protein and other pro-survival genes like cyclin D1 (cyc D1), survivin and hTERT (human telomerase reverse transcriptase) |
| 25572145 | Concomitantly, E2 + TNF-alpha combination increased the survival of SiHa cells by positive changes in viability, proliferation and colony formation |
| 25572145 | E2-induced apoptotic tendency shifted towards senescence in presence of TNF-alpha by arresting the cells at both G0/G1 and G2/M phases, thus enhancing cell survival |
| 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 |
| 25572145 | Our data provide a mechanistic basis and a new insight for the role of TNF-alpha and E2 in linking cellular senescence, tumorigenesis and HPV re-infection |
| 25407919 | ARHGAP18 overexpression induced a predominantly anti-inflammatory senescent population and depletion of the caveolae-associated proteins resulted in the preferential reduction in this senescent population as measured by neutrophil adhesion and adhesion protein expression after TNFalpha treatment |
| 25342130 | Stimulation of endothelial cells (ECs) with TNF-alpha causes an increase in the expression of bone morphogenetic protein-2 (BMP-2) and the production of endothelial microparticles (EMPs) |
| 25341065 | OBJECTIVES: Given their common effects, this study investigated whether A1AT acts via PP2A to alter tumor necrosis factor (TNF) signaling, inflammation, and proteolytic responses in this disease |
| 25341065 | PP2A was silenced in lung epithelial cells treated with A1AT and matrix metalloproteinase and cytokine production was then measured following TNF-alpha stimulation |
| 25341065 | CONCLUSIONS: Together, these data indicate that A1AT modulates PP2A to counter inflammatory and proteolytic responses induced by TNF signaling in the lung |
| 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 |
| 25090227 | Among the anti-inflammatory cytokines, the production of prostaglandin E2 (PGE2) and the expression of its primary enzyme, cyclooxygenase-2 (COX-2), were profoundly increased by pre-stimulation with interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), and this response was significantly decreased with consecutive passages |
| 25083993 | Despite their apparent senescent state, we determined that these cells secreted high levels of both TNF-alpha and IFN-gamma and showed potent cytotoxic activity |
| 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 |
| 24666525 | Pretreatment with 17beta-estradiol or genistein inhibited BAEC senescence induced by male or female db/db LDL and downregulated the expression of lectin-like oxidized LDL receptor-1 and tumor necrosis factor-alpha protein |
| 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 |
| 24481487 | The two-way ANOVA of TNF-alpha levels revealed a significant exercise x caffeine interaction (F (1, 16) = 9 |
| 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 |
| 24286133 | A complex interaction between Wnt signaling and TNF-alpha in nucleus pulposus cells |
| 24286133 | INTRODUCTION: Increased expression of the proinflammatory cytokine TNF-alpha in intervertebral discs (IVDs) leads to inflammation, which results in progressive IVD degeneration |
| 24286133 | However, it is not known whether cross talk between TNF-alpha and Wnt signaling plays a role in the regulation of nucleus pulposus cells |
| 24286133 | The goal of the present study was to examine the effect of the interaction between Wnt signaling and the proinflammatory cytokine TNF-alpha in nucleus pulposus cells |
| 24286133 | METHODS: Cells isolated from rat nucleus pulposus regions of IVDs were cultured in monolayers, and the expression and promoter activity of Wnt signaling and TNF-alpha were evaluated |
| 24286133 | We also examined whether the inhibition of Wnt signaling using cotransfection with Dickkopf (DKK) isoforms and Sclerostin (SOST) could block the effects of pathological TNF-alpha expression in nucleus pulposus cells |
| 24286133 | RESULTS: TNF-alpha stimulated the expression and promoter activity of Wnt signaling in nucleus pulposus cells |
| 24286133 | In addition, the activation of Wnt signaling by 6-bromoindirubin-3'-oxime (BIO), which is a selective inhibitor of glycogen synthase kinase 3 (GSK-3) activity that activates Wnt signaling, increased TNF-alpha expression and promoter activity |
| 24286133 | Conversely, the suppression of TNF-alpha promoter activity using a beta-catenin small interfering RNA was evident |
| 24286133 | Moreover, transfection with DKK-3, DKK-4, or SOST, which are inhibitors of Wnt signaling, blocked Wnt signaling-mediated TNF-alpha activation; these effects were not observed for DKK-1 or DKK-2 |
| 24286133 | CONCLUSIONS: Here, we have demonstrated that Wnt signaling regulates TNF-alpha and that Wnt signaling and TNF-alpha form a positive-feedback loop in nucleus pulposus cells |
| 24286133 | The results of the present study provide in vitro evidence that activation of Wnt signaling upregulates the TNF-alpha expression and might cause the degeneration of nucleus pulposus cells |
| 24269635 | In cultured chondrocytes, IL-1beta and TNF-alpha suppressed FOXO1, while TGF-beta and PDGF increased FOXO1 and FOXO3 expression |
| 24063161 | At 24 hours, 72 hours, and 6 days after culture, the cell morphology and density were observed by inverted microscope; the cell proliferation was assessed by MTT; after 6 days of culture, the cell cycle by propidium iodide staining and flow cytometry, the apoptosis by acridine orange/ ethidium bromide staining, and the cell senescence by beta-galactosidase staining; the levels of tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1), platelet-derived growth factor (PDGF), and insulin-like growth factor 1 (IGF-1) in serum were detected by a double-antibody sandwich ELISA kit |
| 24063161 | The levels of TNF-alpha, IL-1, PDGF, and IGF-1 in group C were significantly higher than those in group B (P < 0 |
| 23952478 | Morin significantly decreased the production of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in the UVB-irradiated KSC |
| 23940580 | A higher influx of F4/80(+) macrophages and CD4(+) T lymphocytes is measured and is accompanied by increases in mRNA of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) |
| 23853351 | The increased susceptibility of immune inflammatory response, morbidity and mortality in the elderly is often associated with decreased frequencies of anti-inflammatory factor IL-10 -1082G allele, TNF-beta1 haplotype cnd10T/C, cnd25G/G, -988C/C, -800G/A, low proinflammatory fator TNFa level related extended TNF-A genotype -1031C/C, -863C/A, -857C/C, IL-6-174 CC and IFN-gamma+874 T allele as well |
| 23611899 | For the next 9 days, the cells were cultured in chondrogenic medium containing 50% conditioned medium derived from C2C12 muscle cells or fibroblast control cells, and were subject to treatments of pro-inflammatory cytokines IL-1beta or TNFalpha |
| 26201620 | Examples include the HLA class-II region and genes implicated in IL12-JAK/STAT signaling, and the NF-kappaB and TNF signaling pathways |
| 23438440 | A role for TNFalpha in intervertebral disc degeneration: a non-recoverable catabolic shift |
| 23438440 | Whole bovine discs were cultured to examine cellular (anabolic/catabolic gene expression, cell viability and senescence using beta-galactosidase) and structural (histology and aggrecan degradation) changes in response to TNFalpha treatment |
| 23438440 | Control or TNFalpha cultures were assessed at 7 and 21 days; the 21 day group also included a recovery group with 7 days TNFalpha followed by 14 days in basal media |
| 23438440 | TNFalpha induced catabolic and anti-anabolic shifts in the nucleus pulposus (NP) and annulus fibrosus (AF) at 7 days and this persisted until 21 days however cell viability was not affected |
| 23438440 | Data indicates that TNFalpha increased aggrecan degradation products and suggests increased beta-galactosidase staining at 21 days without any recovery |
| 23438440 | TNFalpha significantly reduced anabolism in cultured IVDs and a possible mechanism may be associated with cell senescence |
| 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 |
| 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 |
| 23272236 | To confirm selectivity of the SASP-RAP response, cells were treated with senescence-related and -unrelated stimuli (IL-1beta, LPS, TNF-alpha and TGF-beta), and induction of senescence markers and activity of SASP-RAP were evaluated in parallel |
| 23013131 | The p21-induced senescent cells express higher levels of apoptotic cytokines, such as tumour necrosis factor (TNF)-alpha compared with non-senescent cells |
| 23013131 | Exposure of cells to aldosterone for 3 or 5 days increased senescence-associated beta-galactosidase staining, p21 and TNF-alpha mRNA expression and secretion of TNF-alpha into the culture medium |
| 23013131 | A neutralizing antibody against TNF-alpha prevented the aldosterone-induced apoptotic changes |
| 23013131 | These findings indicate that aldosterone increases TNF-alpha synthesis and secretion in proximal tubular cells via p21/senescence-dependent cell phenotypic changes and that the TNF-alpha secreted plays an important role as a paracrine factor in mediating cell apoptosis, indicating a possible involvement in aldosterone-induced renal damage |
| 23000105 | Senescence was also obtained by exposure to TNFalpha, which causes cell changes resembling cellular senescence |
| 23000105 | Klotho was also reduced in cells exposed to the proinflammatory cytokine TNFalpha |
| 23000105 | The addition of exogenous Klotho to aging cells did not modify the proportion of cells with short telomeres or any other feature of cell aging; however, exogenous Klotho prevented the changes resembling premature cellular senescence associated with TNFalpha, such as the decrease in telomere length and the increase in beta-galactosidase-positive cells |
| 23000105 | Likewise exogenous Klotho prevented the increases in reactive oxygen species (ROS) activity, mitochondrial potential and cell apoptosis induced by TNFalpha |
| 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 |
| 22252437 | We have recently published that the proinflammatory cytokine TNFalpha is a strong inducer of CD4(+) T-cell senescence and T-cell differentiation, adding to the growing body of literature implicating proinflammatory molecules in mediating these critical age-related T-cell alterations |
| 21985896 | Based on increases in SMalphaA, stimulation with the proinflammatory cytokine tumor necrosis factor-alpha, but not with TGF-beta, induced EnMT in early passage cells similar to that observed in late passage cells |
| 21738489 | Here we map Sirt6 occupancy on mouse promoters genome-wide and show that Sirt6 occupancy is highly dynamic in response to TNF-alpha |
| 21698300 | Compared to early cultures, late passage HUVECs also exhibited nuclear translocation of NF-kappaB (p65) and reciprocal shifts in BAX and BCL2 protein content resulting in almost 2-fold increase in BAX/BCL2 ratio and 3-fold increase in apoptotic response to TNFalpha exposure (p<0 |
| 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 | 83) or only TNF-alpha 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 |
| 21562872 | RESULTS: In Ovx mice, Med/E2 at their respective osteoprotective doses resulted in thymus involution and lowered Ovx-induced increase in serum TNF-alpha level and its mRNA levels in the BM T cells |
| 21212468 | Zfra (zinc finger-like protein that regulates apoptosis) is a naturally occurring short peptide consisting of 31 amino acids, which regulates tumor necrosis factor (TNF)-mediated cell death by interacting with receptor adaptor protein TRADD (TNF receptorassociated death domain protein) and downstream JNK (c-Jun N-terminal kinase), NF-kappaB (Nuclear factor kappa B) and WWOX/WOX1 (WW domain-containing oxidoreductase) |
| 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 | Abuse was associated with heightened IL-6 and TNF-alpha levels; for TNF-alpha, this relationship was magnified in caregivers compared with controls |
| 24281089 | Proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma, as well as chemokines and prostaglandins, are synthesized by resident brain cells and lymphocytes invading the affected brain tissue |
| 20016203 | The basal and stimulated (by TNF-alpha) levels of NFkappaB were augmented in senescent cells in electrophoretic mobility shift assays in association with increased oxidative stress, increased p53 protein stability, and activated apoptotic pathways |
| 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 |
| 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 |
| 19124561 | We therefore studied the senescence of proliferative human EPCs and investigated the effects of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) on their senescence |
| 19124561 | However, EPCs up-regulated the expression of the senescence-associated cell cycle arrest protein p16(INK4a) and markedly increased measured senescence levels when exposed to chronic TNF-alpha treatment |
| 18180277 | OBJECTIVES: To study the clinical outcome, treatment response, T-cell subsets and functional consequences of a novel tumour necrosis factor (TNF) receptor type 1 (TNFRSF1A) mutation affecting the receptor cleavage site |
| 18180277 | Apoptosis of PBMCs was studied by stimulation with TNFalpha in the presence of cycloheximide and annexin V staining |
| 18178582 | Pathway analysis of the differently regulated proteins suggests an increase in p53 activity in the p53(K317R) thymocytes as well as a decrease in tumor necrosis factor alpha signaling |
| 17785865 | Correspondingly, caregivers had significantly lower T cell proliferation but higher production of immune-regulatory cytokines (TNF-alpha and IL-10) than controls in response to stimulation in vitro |
| 17202338 | To support this hypothesis, we show here that the reduction of Klotho expression and activity in both elderly and patients' lymphocytes occurs in concert with the down-regulation of T cell costimulatory molecule CD28, the latter known to be dependent on increased levels of TNF-alpha |
| 17199788 | Serum oxidized low-density lipoprotein (ox-LDL), tumour necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) were also measured in both groups by ELISA |
| 17199788 | TNF was also inversely associated with percentage telomerase activity in the whole group studied (r = -0 |
| 17199788 | In stepwise multiple linear regression, taking into consideration the most important characteristics of the HD patients and control group, the only significant predictors for percentage telomerase activity in PBMC were ox-LDL and TNF (beta = -0 |
| 17142862 | The upregulation of the transcription factor nuclear factor kappaB (NF-kappaB) in transformed hepatocytes, through the paracrine action of tumor necrosis factor-alpha from neighboring endothelia and inflammatory cells, may be critical for tumor progression given the mitogenic and anti-apoptotic properties of proteins encoded by many of NF-kappaB's target genes |
| 16930678 | In this report, ICAM-1 accumulates in late passage endothelial cells when compared to early passage endothelial cells, yet ICAM-1 protein expression is attenuated when senescent cells are challenged by TNF-alpha (10ng/ml) |
| 16300653 | Up-regulation of the transcription factor NF-kappaB in transformed hepatocytes, through the paracrine action of TNF-alpha from neighbouring endothelia and inflammatory cells, may be critical for tumour progression given the mitogenic and antiapoptotic properties of proteins encoded by many of NF-kappaB's target genes |
| 15130673 | Cell death following stimulations: (i) corresponded to apoptosis, associated with necrosis at the end of the culture; (ii) was not, for its main part, mediated through CD95/CD178 or TNFRII/TNF alpha interactions; and (iii) occurred in spite of bcl-2 increased expression |
| 13679081 | Matrix metalloproteinase-9 (MMP-9) expression was also increased in response to tumor necrosis factor-alpha (TNF-alpha) in aged MASMC, as evidenced by zymography and immunoblot analysis |
| 13679081 | Transient transfection assays showed an age-dependent increase in transcription from MMP-9 promoter activity in response to TNF-alpha |
| 12569699 | The hTERT positive fibroblasts could form bone nodules when they were cultured in vitro induced by bone morphogentic protein 2 and tumor necrosis factor-alpha |
| 11855860 | We have found that human senescent fibroblasts can be induced to undergo programmed cell death (apoptosis) by ceramide, TNF-alpha, or okadaic acid |
| 11855860 | The most profound effects were induced by TNF-alpha and okadaic acid treatment |
| 11855860 | TNF-alpha was the only agent that induced lysosomal activity in senescent fibroblasts, of which only alpha-galactosidase A activity was induced |
| 11828880 | Energetic stress in combination with tumor necrosis factor-alpha (TNF-alpha) induces apoptosis of human fibroblasts (WI-38) in vitro: reduced responsiveness of senescent cells |
| 11828880 | 4%) under treatment with either a high-NaCl medium or TNF-alpha (10 nM) alone, combined treatment resulted in a strong increase in Phase II cells and a significantly lesser rise in the case of "senescent" Phase III cells |
| 11828880 | We conclude, therefore, that energetic stress stimulates sensitivity to apoptosis by (in the presence of) TNF-alpha, especially pronounced in potentially replicating "young" as compared with irreversible postmitotic ("senescent") fibroblasts |
| 11679409 | To investigate a specific function modulated by endothelial NO, adhesion of monocytes under basal conditions as well as after exposure to TNF-alpha was assessed |
| 11679409 | Exposure of TNF-alpha resulted in a 2-fold increase in monocyte adhesion in senescent cells, whereas this effect was reduced in cells transfected with hTERT |
| 11480555 | Ceramide levels are elevated in response to diverse stress challenges including chemotherapeutic drug treatment, irradiation, or treatment with pro-death ligands such as tumor necrosis factor alpha, TNF alpha |
| 10094826 | Transient transfection assays with TK5-CAT and TK10-CAT plasmids carrying NF-kappaB-responsive sites of the TNFalpha promoter were used to analyze the functional activity of the NF-kappaB complexes |
| 8688670 | CD95 (APO-1) is a member of the TNF/nerve growth factor receptor superfamily, which is expressed on the surface of different types of cells |
| 7561522 | In addition, lipopolysaccharide (LPS) was synergistic with IL-1 beta or tumor necrosis factor-alpha (TNF-alpha) in induction of nitric oxide synthesis |
| 7561522 | Rat and mouse fibroblasts were also found to produce nitric oxide when primed with IFN-gamma and simultaneously treated with IL-1, TNF-alpha, or LPS |
| 7561522 | Furthermore, effective triggering doses of LPS, TNF-alpha, and IL-1 were 10 ng/ml, 100 U/ml, and 0 |
| 7561522 | At the stage of growth crisis, a dramatic increase in nitric oxide production was observed in rat fibroblasts in response to IFN-gamma or TNF-alpha that may be directly correlated with cellular senescence |
| 7737374 | The short-term growth of these cells in culture is regulated by a number of different cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and fibroblast growth factor (FGF) |
| 7737374 | In the present report, we examined the effects of TNF on foreskin-derived HDF at different passage levels |
| 7737374 | Young cells proliferated in response to TNF in a dose-dependent manner |
| 7737374 | Under these conditions TNF had no effect on senescent HDF |
| 7737374 | The decrease in TNF responsiveness was found to be dependent on PD |
| 7737374 | The lack of response of senescent HDF was not unique to TNF, since FGF and IL-1 were also ineffective |
| 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 |
| 7737374 | The diminished responsiveness of senescent HDF to TNF does not appear to be due to the difference in either receptor number or affinity, since senescent cells had two- to threefold higher number of TNF receptors than young HDF but the same affinity |
| 7737374 | TNF induced the activation of a nuclear transcriptional factor, NF-kappa B, equally in both young and senescent cells, which indicates the lack of a defect in the early events of TNF signal transduction in senescent fibroblasts |
| 7737374 | Overall, our results indicate that there is an age-dependent decline in TNF-induced proliferation and in the production of interleukins by fibroblasts; this unresponsiveness appears not to be due to TNF receptors or NF-kappa B activation |
| 7862174 | Arguments will then be developed in favor of the implication of the ROS in the cellular effects of PMA, TNF-alpha and other cytokines on the modulation of the genetic expression |
| 8262134 | We have studied changes in gene expression induced in these cells following exposure to the cytokine, tumor necrosis factor-alpha (TNF) |
| 8359220 | Here we show that (i) senescence enhances monoblastoid U937 cell adhesion to the endothelial monolayer; (ii) the enhanced interaction between senescent endothelial cells and U937 cells is mediated, at least in part, by the overexpression of ICAM-1; and (iii) LPS and interleukin 1 alpha, but not tumor necrosis factor alpha, are unable to stimulate the adhesion of U937 to senescent endothelial cells |
| 8376318 | Tumor necrosis factor-alpha (TNF) and various interferons (IFN) have potent cytostatic or cytotoxic effects on a variety of human tumor-derived cell lines |
| 8376318 | We have examined the effects of TNF and IFN-beta on the proliferation of WI-38 cells in a serum-free, growth factor-supplemented medium and in serum-containing medium |
| 8376318 | TNF has no effect on this growth factor-stimulated proliferation |
| 8376318 | TNF and IFN-beta together have a synergistic effect and completely inhibit growth factor-stimulated DNA synthesis in young cells |
| 8376318 | TNF stimulated an increase in the number of EGF specific binding sites two- to threefold in 24 h in both young and senescent cells |
| 8376318 | IFN-beta has little or no effect on EGF binding either alone or in combination with TNF |
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