| 27306980 | Cells undergoing senescence acquire a senescence associated secretory phenotype (SASP) leading to the production of interleukin-1 alpha (IL-1alpha), which has been implicated in several degenerative and inflammatory processes including renal disease |
| 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 |
| 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 |
| 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 |
| 25156255 | Mechanistically, we found that Gr-1(+) cells antagonize senescence in a paracrine manner by interfering with the senescence-associated secretory phenotype of the tumour through the secretion of interleukin-1 receptor antagonist (IL-1RA) |
| 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 |
| 23770676 | Expression of the SASP is controlled by inflammasome-mediated IL-1 signalling |
| 23770676 | The inflammasome and IL-1 signalling are activated in senescent cells and IL-1alpha expression can reproduce SASP activation, resulting in senescence |
| 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) |
| 23385065 | IL1 shared features of replicative, oncogene-induced, and drug-induced paracrine 'bystander senescence' |
| 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 | Persistent cytokine signaling and activated DDR evoke senescence in normal bystander cells, accompanied by activation of the JAK/STAT, TGFbeta/SMAD and IL1/NFkappaB signaling pathways |
| 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 |
| 23385065 | Furthermore, the observed IL1- and TGFbeta-induced expression of NAPDH oxidase Nox4 indicates a mechanistic link between the senescence-associated secretory phenotype (SASP) and DNA damage signaling as a feature shared by development of all major forms of paracrine bystander senescence |
| 22692818 | Mimic and antagomir transfection confirmed TLR's IL-1 receptor-associated kinase (IRAK1) protein modulation in both young and senescent cells |
| 22454193 | METHODS: Isolated chondrocytes were cultured in medium containing interleukin-1 beta (IL-1beta) with or without Rg3 |
| 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 |
| 19802007 | Furthermore, cytokine genes, including proinflammatory IL1, tumor necrosis factor and transforming growth factor families, were highly expressed |
| 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 |
| 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 |
| 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 |
| 10379796 | Interleukin-1 levels were depressed after surgical menopause but not as much as found in the old menopausal females and this low level was not corrected by hormonal replacement |
| 10379796 | CONCLUSIONS: The deficient Il-1, Il-2 and antibody response following infection was not corrected by hormone replacement and thus appears to be due to aging rather than lack of female hormones |
| 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 | Although interleukin-1 beta stimulated cell growth in five of six patients, the differences observed were not statistically significant |
| 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 |
| 9255759 | The enhancement of LPS-stimulated PGE2 production was inhibited by anti-IL-1 beta antibody and by IL-1 receptor antagonist |
| 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 |
| 9207769 | IL-1 beta-converting enzyme mRNA remained unchanged |
| 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 |
| 8972724 | The human diploid fibroblast senescence pathway is independent of interleukin-1 alpha mRNA levels and tyrosine phosphorylation of FGFR-1 substrates |
| 8972724 | In vitro cellular senescence of human umbilical vein endothelial cells (HUVEC) may involve the intracellular activity of the signal peptide-less cytokine interleukin (IL)-1 alpha |
| 8972724 | To determine whether senescence of other human diploid cells involves the function of IL-1 alpha, we examined the steady-state expression of IL-1 alpha mRNA in IMR-90 fibroblasts |
| 8972724 | The IL-1 alpha transcript was not elevated in senescent IMR-90 cells |
| 8972724 | With the exception of the plasminogen activator inhibitor (PAI)-1 transcript, other IL-1 alpha-response gene mRNAs were not induced in senescent IMR-90, although the mRNA for each gene was induced by exogenous IL-1 alpha |
| 8972724 | These data demonstrate that IL-1 alpha and FGF-1 may have different functions in HUVEC and IMR-90 fibroblast populations including distinct pathways for the regulation of cellular growth and senescence |
| 8806439 | Modulation of hemopoietic factor production in relation to endothelial cell aging by interleukin-1 induction |
| 8806439 | In this study, we examined the modulation of hemopoietic factor production by human umbilical vein endothelial cells in relation to aging and the cell cycle under conditions of interleukin-1 (IL-1) induction and noninduction |
| 8806439 | Under conditions of IL-1 noninduction, messenger RNA expression levels of macrophage colony-stimulating factor (M-CSF) were three times higher in non-S-phase cells of young cultures than those in S-phase cells |
| 8806439 | Under conditions of IL-1 induction G-CSF and M-CSF expression levels were enhanced in both young and old cells |
| 8549657 | We demonstrated that in comparison with early passage cultures the expression of collagenase and stromelysin mRNAs and proteins was increased > 8 x in late passage cultures of human fibroblasts and, in addition, expression of Il-1 alpha, a cytokine that regulates collagenase and stromelysin expression, was also significantly increased in late passage cell cultures |
| 8549657 | These findings suggested the hypothesis that constitutive Il-1 alpha expression in late passage cells may coordinately regulate the age-associated increase in the expression of collagenase and stromelysin |
| 8549657 | To test this hypothesis we examined the effects of long-term Il-1 alpha treatment, serum starvation, and cycloheximide inhibition on collagenase and stromelysin mRNA levels in early and late passage human fibroblast cell cultures |
| 8549657 | Here we report that in late passage cell cultures, collagenase and stromelysin mRNAs respond differentially to Il-1 alpha, serum starvation, and cycloheximide addition |
| 8549657 | Continuous exposure to Il-1 alpha reduced the half-life of stromelysin mRNA but had little effect on the half-life of collagenase mRNA |
| 8549657 | In addition, these studies support the conclusion that continuous long-term exposure to Il-1 alpha, a condition that is characteristic of late passage cells, is not the factor responsible for the high levels of collagenase expression, but may be critical for stromelysin expression |
| 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 |
| 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 |
| 7628547 | Interestingly the increase of PAI-1 levels correlates with the upregulation of interleukin 1 alpha, which characterizes endothelial cell senescence |
| 7628547 | Moreover, PAI-1 was not upregulated in senescent or in progeric human fibroblasts, which do not overexpress interleukin 1 alpha, thus suggesting that multiple pathways may exist to regulate aging of human fibroblasts and endothelial cells |
| 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 | The lack of response of senescent HDF was not unique to TNF, since FGF and IL-1 were also ineffective |
| 7737374 | In contrast to senescent HDF, TNF-dependent proliferation of young HDF could be further potentiated by IL-1 and FGF, suggesting an independent signaling mechanism |
| 8114717 | Endogenous interleukin 1 alpha must be transported to the nucleus to exert its activity in human endothelial cells |
| 8114717 | We have previously shown that the signal peptideless cytokine interleukin 1 alpha (IL-1 alpha) may play a role as an intracellular regulator of human endothelial cell senescence (J |
| 8114717 | To investigate the potential intracellular function of IL-1 alpha, transformed endothelial cells were transfected with the human cDNAs that code for the two forms of IL-1 alpha, the precursor molecule IL-1(1-271) and the mature protein IL-1(113-271) |
| 8114717 | The subcellular localization of the two different polypeptides was investigated directly or by using chimeric genes constructed by fusion of different fragments of the IL-1 alpha gene and the beta-galactosidase open reading frames |
| 8114717 | The basic cluster at the NH2 terminus of IL-1, KVLKKRR, has been shown to mediate IL-1 alpha nuclear targeting |
| 8114717 | Moreover, nuclear localization of IL-1 alpha correlates with impaired cell growth and expression of some IL-1 alpha-inducible genes |
| 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 |
| 1322316 | Interleukin-1 alpha treatment increased collagenase and stromelysin mRNA levels while transforming growth factor-beta reduced the steady-state levels of both transcripts |
| 1716619 | Epidermal growth factor and its receptor, basic fibroblast growth factor, transforming growth factor beta-1, and interleukin-1 alpha messenger RNA production in human corneal endothelial cells |
| 1716619 | The authors tried to determine whether human corneal endothelial cells in primary culture synthesize messenger RNA (mRNA) coding for epidermal growth factor (EGF), EGF receptor, basic fibroblast growth factor (FGFb), transforming growth factor beta-1 (TGFb1), and interleukin-1 alpha (IL-1 alpha) |
| 1716619 | The polymerase chain reaction (PCR) was used to amplify the growth factors (EGF, FGFb, TGFb1, and IL-1 alpha), EGF receptor, and beta actin sequences from each of the cDNA samples |
| 1716619 | The EGF mRNAs were detected by PCR alone in four of the samples from proliferative cultures, TGFb1 mRNAs in three, and IL-1 alpha mRNAs in three |
| 2218499 | Extension of the life-span of human endothelial cells by an interleukin-1 alpha antisense oligomer |
| 2218499 | Senescent human endothelial cells were shown to contain high amounts of the transcript for the cytokine interleukin-1 alpha (IL-1 alpha), a potent inhibitor of endothelial cell proliferation in vitro |
| 2218499 | In contrast, transformed human endothelial cells did not contain detectable IL-1 alpha messenger RNA |
| 2218499 | Treatment of human endothelial cell populations with an antisense oligodeoxynucleotide to the human IL-1 alpha transcript prevented cell senescence and extended the proliferative life-span of the cells in vitro |
| 2218499 | Removal of the IL-1 alpha antisense oligomer resulted in the generation of the senescent phenotype and loss of proliferative potential |
| 2218499 | These data suggest that human endothelial cell senescence in vitro is a dynamic process regulated by the potential intracellular activity of IL-1 alpha |
