| 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 |
| 27812125 | Genes-toll-interacting protein (TOLLIP), mitogen-activated protein kinase 9 (MAPK9), interleukin-1beta (IL-1beta), interleukin-8 (IL-8), and chemokine (C-X-C motif) ligand 1 (CXCL1)-related to these two pathways were validated using western blotting |
| 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 |
| 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 |
| 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 |
| 26341894 | Interleukin-1beta in intervertebral disk degeneration |
| 26341894 | Interleukin-1 (IL-1) beta is the most important member of the IL-1 family, and has a strong pro-inflammatory activity by stimulating the secretion of multiple pro-inflammatory mediators |
| 26341894 | IL-1beta is highly expressed in degenerative intervertebral disk (IVD) tissues and cells, and it has been shown to be involved in multiple pathological processes during disk degeneration, including inflammatory responses, matrix destruction, angiogenesis and innervation, cellular apoptosis, oxidative stress and cellular senescence |
| 26341894 | However, inhibition of IL-1beta is found to promote extracellular matrix (ECM) repair and protect against disk regeneration |
| 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 experiments used IL-1beta- or TNF-alpha-treated human annulus cells to test for autophagy-related gene expression |
| 26091153 | In vitro data suggested a mechanism implicating a role of TNF-alpha and IL-1beta in disc autophagy |
| 25989853 | However, pathological stabilization of the actin cytoskeleton increased LPS-induced release of IL-1beta and IL-18, which belong to an unconventional secretory pathway |
| 25894557 | These senescent cells expressed proinflammatory cytokines such as interleukin-1beta (IL-1beta) |
| 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 |
| 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 |
| 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 |
| 25186470 | Gene and protein expression of antioxidant proteins and autophagy-related proteins and changes in inflammatory mediators following treatment with interleukin-1beta were assessed |
| 25087910 | We sought to explore whether glucosamine can activate autophagy in rat nucleus pulposus (NP) cells and protect cells treated with IL-1beta or hydrogen peroxide (H2 O2 ) |
| 25087910 | Autophagy in IL-1beta or H2 O2 -treated cells was increased by glucosamine |
| 25087910 | Glucosamine attenuated the decrease of aggrecan and prevented the apoptosis of the NP cells induced by IL-1beta, whereas 3-MA partly reversed these effects |
| 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 |
| 24964749 | Inhibiting ERCC1 in chondrocytes under interleukin-1beta stimulation using small interfering RNA (siRNA) was also evaluated |
| 24964749 | ERCC1 expression was decreased in OA cartilage and increased within 4 h of exposure to interleukin (IL)-1beta, but decreased after 12 h |
| 24801508 | Measurement of secreted factors showed that E-CSC release larger amounts of proinflammatory cytokine IL1beta compared with D-CSC |
| 24801508 | Using blocking antibodies, we verified that IL1beta hampers the paracrine protective action of E-CSC on cardiomyocyte viability |
| 24801508 | IL1beta acts intracranially inducing IKKbeta signaling, a mechanism that via nuclear factor-kappaB upregulates the expression of IL1beta itself |
| 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 pro-inflammatory cytokine levels demonstrated a significant exercise x caffeine interaction for IL-1beta (F (1, 16) = 9 |
| 24269635 | In cultured chondrocytes, IL-1beta and TNF-alpha suppressed FOXO1, while TGF-beta and PDGF increased FOXO1 and FOXO3 expression |
| 24269635 | FOXO1 and FOXO3 phosphorylation was increased by IL-1beta, PDGF, bFGF, IGF-1, and the oxidant t-BHP |
| 24198727 | In addition, both treatments induced the expression of a variety of cytokines, including interleukin-1beta (IL-1beta) and nerve growth factor (NGF) |
| 24198727 | AdRas12V infection induced IL-1beta expression more significantly than H(2)O(2) treatment, whereas both treatments induced comparable mRNA and protein expression levels of NGF |
| 24086293 | Human fibroblasts from four donors were cultured for 90 days in: 1) medium lacking ascorbic acid only, 2) 10 mM buthionine sulphoximine (BSO) (pro-oxidant), 3) 25 mM D-glucose, 4) 1 ng/ml IL1B and 5) 25 mM D-glucose+1 ng/ml IL1B |
| 24086293 | Cultures treated with high glucose and BSO displayed a significantly lower growth rate, and cultures treated with IL1B showed a trend towards a higher growth rate, compared to the control [Glucose:0 |
| 24086293 | Telomere shortening with time was significantly accelerated in cultures treated with IL1B compared to the control [IL1B:-0 |
| 24086293 | The hastening of telomere shortening by IL1B was only in part attenuated after adjustment for the number of cell divisions [IL1B:-4 |
| 23952478 | Morin significantly decreased the production of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in the UVB-irradiated KSC |
| 23864729 | Activation of the AIM2 inflammasome cleaves pro-interleukin (IL)-1beta and pro-IL-18 and promotes the secretion of IL-1beta and IL-18 proinflammatory cytokines |
| 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 |
| 23611899 | RESULTS: Both IL-1beta and TNFalpha-induced strong expression of multiple MMPs and hypertrophic markers Runx2 and type X collagen |
| 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 |
| 22454193 | METHODS: Isolated chondrocytes were cultured in medium containing interleukin-1 beta (IL-1beta) with or without Rg3 |
| 22454193 | RESULTS: Chondrocytes stimulated by IL-1beta showed increased MMP-1, MMP-3, and MMP-13 levels, whereas the expression of COL2A1 and ACAN decreased |
| 22454193 | However, in cells co-treated with IL-1beta and Rg3, the levels of MMP-1 and MMP-13 were lower than in cells treated with IL-1beta alone, and COL2A1 and ACAN expression levels recovered from the low values seen when cultured only in the presence of IL-1beta |
| 22454193 | Also, compared to vehicle-treated controls, IL-1beta stimulation alone resulted in an increased number of SA-beta-Gal-positive cells, while co-incubation with IL-1beta and Rg3 significantly suppressed the expression of this senescence marker |
| 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 |
| 21471287 | On sensing dsDNA, the IFI16 protein induces the expression of IFN-beta whereas the AIM2 protein forms an inflammasome, which promotes the secretion of IL-1beta |
| 21471287 | Accordingly, increased constitutive levels of IFI16 and AIM2 proteins in ataxia telangiectasia mutated (ATM) HDFs were associated with the activation of the IFN signaling and increased levels of IL-1beta |
| 21471287 | The IFN-beta treatment of the young HDFs, which induced the expression of IFI16 and AIM2 proteins, activated a DNA damage response and also increased basal levels of IL-1beta |
| 21224216 | The changes of SIRT6, p21, and interleukin (IL)-1beta expression levels in HBEC, as well as type I collagen expression levels in fibroblasts, were evaluated |
| 21224216 | TGF-beta-induced senescent HBEC secreted increased amounts of IL-1beta, which was sufficient to induce myofibroblast differentiation in fibroblasts |
| 21098883 | The OA-related catabolic factor, IL-1beta induced marked downregulation of cellular activity, expression of a senescent biomarker, specific senescence-associated beta-galactosidase activity and shortening of the cellular lifespan in chondrocytes |
| 20374325 | Chondrocytes were stimulated with or without IL-1beta (10 ng/mL) in the presence or absence of vascular endothelial growth factor, basic fibroblast growth factor or hepatocyte growth factor (20 ng/mL) |
| 20374325 | IL-1beta significantly decreased the cellular replicative lifespan in chondrocytes |
| 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 |
| 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 |
| 16508959 | This study was undertaken to investigate whether the catabolic factors oxidative stress and interleukin-1beta (IL-1beta) induce features of premature senescence of articular chondrocytes through up-regulation of caveolin 1 expression |
| 16508959 | We studied whether IL-1beta and H2O2 induce caveolin 1 expression in OA chondrocytes and analyzed the relationship between cellular senescent phenotypes and caveolin 1 expression in human chondrocytes |
| 16508959 | Both IL-1beta and H2O2 up-regulated caveolin 1 messenger RNA and protein levels, and both treatments induced marked expression of senescent phenotypes: altered cellular morphology, cell growth arrest, telomere erosion, and specific senescence-associated beta-galactosidase activity |
| 16508959 | CONCLUSION: Our findings suggest that IL-1beta and oxidative stress induce features of premature senescence in OA chondrocytes, mediated, at least in part, by stress-induced caveolin 1 expression |
| 16419088 | In the current study we examined long-term effects of antioxidants vitamin E and alpha-lipoic acid on cultured rat microglia with respect to proliferative ability, telomere length, telomerase activity, and interleukin-1beta (IL-1beta) production |
| 16419088 | Production of IL-1beta was significantly decreased in vitamin E-treated microglia in vitro |
| 15876845 | After culture in vitro, these cells shown increase susceptibility to undergoing spontaneous apoptosis, that is enhanced by IL-4 and prevented by IL-1beta or LPS |
| 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 |
| 15621568 | In conclusion, the functional data identifying a difference in mortalin expression in IL-1beta stimulated islets between two rat strains and over-expression of mortalin in NIH3T3 cells associated with decreased viability suggests a functional role for mortalin in cytokine mediated beta cell destruction; however, the identified polymorphisms did not reveal any association in the presence of linkage disequilibrium of mortalin to T1DM in the Danish population |
| 15388329 | Here, we show that in mouse embryonic fibroblasts (MEFs) culture in vitro, expression of an inflammatory cytokine, interleukin-1beta (IL-1beta) and its antagonist, IL-1 receptor antagonist (IL-1Ra) are induced by senescence |
| 15388329 | Our results suggest that IL-1beta signaling pathway is involved in activation of p38 linked cellular senescence |
| 10433392 | Enhancement of lipopolysaccharide-stimulated PGE2 and IL-1beta production in gingival fibroblast cells from old rats |
| 10433392 | The levels of prostaglandin E2 (PGE2) and interleukin 1beta (IL-1beta) released into the cultured medium were measured by a specific radioimmunoassay |
| 10433392 | LPS stimulated PGE2 and IL-1beta production in a dose-and time-dependent manner in rGF cells from both young and old rats was seen |
| 10433392 | Production of PGE2 and IL-1beta by rGF cells from the old rats was higher than those from the young in response to LPS |
| 10433392 | This greater ability from the older rGF cells to produce PGE2 and IL-1beta was due to higher mRNA levels of cyclooxygenase 2 and IL-1beta, respectively |
| 10433392 | In contrast, cyclooxygenase-1 and IL-1beta converting enzyme gene mRNA levels remained unchanged |
| 10433392 | Because LPS-stimulated PGE2 and IL-1beta production was enhanced by in vivo cellular aging, aging of GF may affect the severity of inflammation and bone resorption by producing a large amount of PGE2 and IL-1beta in response to bacterial infection |
| 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 |
| 9722719 | Cyclic tension force to HPLF also stimulated phenotypic and gene expression of IL-1 beta, PGE2 (COX-2 gene) and tPA |
| 9423715 | In further experimentation, media was supplemented with additional calf serum (20%, 30%, 40%, 50%) and growth factors (epidermal growth factor, basic fibroblast growth factor, interleukin-1 beta) in an attempt to stimulate growth |
| 9423715 | This decreased growth can be stimulated by growth factors basic fibroblast growth factor, epidermal growth factor, and interleukin-1 beta |
| 9255759 | Contribution of IL-1 beta to the enhancement of Campylobacter rectus lipopolysaccharide-stimulated PGE2 production in old gingival fibroblasts in vitro |
| 9255759 | The LPS-stimulated IL-1 beta production in each old cell (corresponding to 57-67% of complete life-span) was increased (1 |
| 9255759 | The IL-1 beta mRNA synthesis in the presence of LPS in the old cells was higher than that in the young cells |
| 9207769 | In vitro cellular aging stimulates interleukin-1 beta production in stretched human periodontal-ligament-derived cells |
| 9207769 | Interleukin (IL)-1 beta is a key mediator involved in periodontal diseases, a potent stimulator of bone resorption |
| 9207769 | To investigate the age-related changes in the biosynthetic capacity of IL-1 beta in PDL cells, we examined the effects of in vitro cellular aging with mechanical stress on IL-1 beta protein and gene expression by human PDL cells |
| 9207769 | We found a two-fold increase in IL-1 beta production by old PDL cells subjected to mechanical tension compared with that by young PDL cells, although the constitutive levels of IL-1 beta were similar in both the young and old PDL cells |
| 9042398 | We also treated early and late passage cells with agents that may modulate the process of cellular senescence: UV light, retinoic acid, and interleukin-1 beta |
| 7561522 | Interleukin-1 beta (IL-1 beta) was found to be the strongest single activator in all types of fibroblasts examined |
| 7561522 | In addition, lipopolysaccharide (LPS) was synergistic with IL-1 beta or tumor necrosis factor-alpha (TNF-alpha) in induction of nitric oxide synthesis |
| 3264123 | Interleukin-1-beta gene expression in human monocytes and alveolar macrophages from normal subjects and patients with sarcoidosis |
| 3264123 | To assess the ability of human alveolar macrophages to produce interleukin-1-beta (IL1-beta), we examined IL1-beta mRNA accumulation in autologous monocytes and alveolar macrophages from normal volunteers |
| 3264123 | Escherichia coli lipopolysaccharide stimulation of monocytes induced rapid IL1-beta mRNA accumulation, reaching a maximum at 2 to 4 h and declining thereafter |
| 3264123 | This difference could not be explained by differences in kinetics of IL1-beta gene expression between the 2 cell types, isolation techniques, or alveolar macrophage lidocaine exposure |
| 3264123 | This suggests that differences in transcription of the IL1-beta gene exist between these 2 cell types |
| 3264123 | To determine if this difference in the capacity to express the IL1-beta gene might be a function of cell maturity, monocytes were aged in vitro for 7 days |
| 3264123 | After this culture period, monocytes had a marked decrease in the ability to accumulate IL1-beta mRNA, suggesting that cell aging may be one mechanism involved in producing these transcriptional differences |
| 3264123 | Because IL1-beta has also been implicated in the inflammatory and fibrotic responses in pulmonary sarcoidosis, 4 patients with newly diagnosed sarcoidosis underwent bronchoalveolar lavage, and IL1-beta mRNA accumulation was compared in their alveolar macrophages and blood monocytes |
| 3264123 | Comparing normal alveolar macrophages to those from patients with sarcoidosis showed no differences in the kinetics of IL1-beta mRNA expression or in the LPS-induced levels of IL1-beta mRNA accumulation |
| 3264123 | In addition, augmented levels of IL1-beta transcript were not noted in unstimulated sarcoid alveolar macrophages |
