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 |
26199639 | Moreover, bavachalcone suppressed senescence in human endothelial cells and mRNA expression of p16(ink4a) (a marker of replicative senescence) and IL-1alpha (a proinflammatory cytokine of the senescence-associated secretory phenotype) |
26147250 | MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation |
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 |
26069700 | The effect of osteogenic protein-1 (OP-1) or interleukin-1alpha (IL-1alpha) treatment on telomerase activity in chondrocytes was also measured to determine the response to anabolic or catabolic stimuli |
26069700 | Chondrocytes from prepubescent horses (<15 months) were treated with OP-1 or IL-1alpha |
26069700 | Treatment with IL-1alpha resulted in a decrease in chondrocyte telomerase activity; however, treatment with OP-1 did not change telomerase activity |
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) |
24434012 | Multiplex analysis revealed that multiple cytokines are increased in BPH, including GM-CSF, IL-1alpha, and IL-4, and that these are also increased in senescent prostatic epithelial cells in vitro |
24434012 | IHC analysis revealed the multifocal epithelial expression of cathepsin D and coexpression with IL-1alpha in BPH tissues |
24434012 | In tissue recombination studies in nude mice with immortalized prostatic epithelial cells expressing IL-1alpha and prostatic stromal cells, both epithelial and stromal cells exhibited increased growth |
24434012 | Expression of IL-1alpha in prostatic epithelial cells in a transgenic mouse model resulted in increased prostate size and bladder obstruction |
24062309 | Redox control of the senescence regulator interleukin-1alpha and the secretory phenotype |
24062309 | IL-1alpha is a key senescence-associated (SA) proinflammatory cytokine that acts as a critical upstream regulator of the SA secretory phenotype (SASP) |
24062309 | We established that SA shifts in steady-state H2O2 and intracellular Ca(2+) levels caused an increase in IL-1alpha expression and processing |
24062309 | The increase in intracellular Ca(2+) promoted calpain activation and increased the proteolytic cleavage of IL-1alpha |
24062309 | Ca(2+) chelation or calpain inhibition prevented SA processing of IL-1alpha and its ability to induce downstream cytokine expression |
24062309 | Collectively, these findings demonstrate how SA alterations in the redox state and Ca(2+) homeostasis modulate the inflammatory phenotype through the regulation of the SASP initiator IL-1alpha, creating a microenvironment permissive to tumor invasion |
23770676 | The inflammasome and IL-1 signalling are activated in senescent cells and IL-1alpha expression can reproduce SASP activation, resulting in senescence |
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 |
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 |
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 |
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 |
16280018 | On the other hand, a significant positive correlation existed between age and interleukin ((IL)-1alpha secretion (R2=0 |
16280018 | The IL-1alpha secretion by keratinocytes was significantly increased in the fifth cultures compared with the second cultures (P<0 |
16280018 | CONCLUSIONS: These findings suggest that IL-1alpha secretion increases as cells grow older, and the increased secretion of IL-1alpha by aged keratinocytes may stimulate HGF production in dermal fibroblasts paracrinely and ET-1 production in keratinocytes autocrinely, which stimulates melanocyte proliferation and induces an increase of tyrosinase activity in melanocytes |
16280018 | Because IL-1alpha is a primary mediator that responds to inflammation and injury, the transcription of genes involved in skin inflammation may be persistently induced in the aged skin |
16280018 | Thus the increased secretion of IL-1alpha by aged keratinocytes in the aged skin may play a role in the accentuated cutaneous pigmentation and other skin ageing |
12640658 | In BPH, there is an increased expression of Il-1alpha by prostatic epithelial cells that results in elevated expression of FGF7 by stromal cells, which in turn is strongly correlated with epithelial proliferation |
12640658 | Il-1alpha expression was localized by immunohistochemistry and Il-1alpha tissue content determined by enzyme-linked immunoabsorption assay |
12640658 | RESULTS: Expression of Il-1alpha is significantly increased in vitro when cultured prostatic epithelial cells undergo senescence |
12640658 | By quantitative assay, SA-beta gal activity is correlated with both tissue levels of Il-1alpha and the severity of BPH |
12640658 | CONCLUSIONS: One mechanism driving BPH in older men is the accumulation of senescent epithelial cells expressing Il-1alpha, which in turn increases FGF7 secretion and proliferation of non-senescent epithelial cells |
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 |
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 |
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 |