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Biochim Biophys Acta. 1996 Nov 8;1314(1-2):109-19.

The human diploid fibroblast senescence pathway is independent of interleukin-1 alpha mRNA levels and tyrosine phosphorylation of FGFR-1 substrates.

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1
Department of Molecular Biology, Holland Laboratory, American Red Cross, Rockville, MD 20855, USA.

Abstract

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. 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. The IL-1 alpha transcript was not elevated in senescent IMR-90 cells. 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. The mRNA expression of cell cycle-specific genes demonstrated that Fos and ornithine decarboxylase (ODC) were induced in young and senescent cells in response to both serum and fibroblast growth factor (FGF)-1. Histone (H)3 mRNA was induced by serum in young cells, but not in senescent cells, and FGF-1 failed to induce H3 mRNA in either young or senescent cells. Further, while young IMR-90 populations were able to respond to serum as an initiator of DNA synthesis and cell growth, they did not exhibit a response to exogenous FGF-1. FGF receptor (R)-1 substrates were not tyrosine phosphorylated in either young or senescent IMR-90 cells. 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.

PMID:
8972724
DOI:
10.1016/s0167-4889(96)00105-x
[Indexed for MEDLINE]
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