Abstract：
:Recent studies have provided evidence that apoptosis of pancreatic beta-cells is important in the early etiology of both type I and type II diabetes mellitus. The mechanisms responsible for induction of apoptosis are unknown, but we present evidence that the signal transduction pathway controlling the process in pancreatic beta-cells is regulated by G-proteins. We have employed the global G-protein activator fluoride and show that this agent induces apoptosis in clonal RINm5F pancreatic beta-cells and also in the cells of normal rat islets of Langerhans. The process is time and concentration dependent and may reflect the formation of AIF4- since it was inhibited by the aluminum chelator deferoxamine. Induction of apoptosis by fluoride was confirmed by acridine orange staining of cell nuclei, by electron-microscopic examination of chromatin condensation, and by oligonucleosomal degradation of DNA. The involvement of G-proteins was confirmed by culture of beta-cells in the presence of pertussis toxin (PTX) prior to exposure to fluoride. PTX did not affect the extent of cell death under control conditions but it consistently, and markedly, enhanced the response to fluoride. The results demonstrate that apoptosis can be induced in pancreatic beta-cells by sustained activation of a G-protein-dependent signaling pathway(s) and they further suggest that a pertussis toxin-sensitive G-protein is involved in attenuation of the response. Treatment of RINm5F pancreatic beta-cells with dibutyrylcAMP resulted in a dose-dependent, saturable increase in cell death, suggesting that a sustained rise in intracellular cAMP may form part of the effector system controlling apoptosis.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Loweth AC,Williams GT,Scarpello JH,Morgan NGdoi
10.1006/excr.1996.0344subject
Has Abstractpub_date
1996-11-25 00:00:00pages
69-76issue
1eissn
0014-4827issn
1090-2422pii
S0014-4827(96)90344-4journal_volume
229pub_type
杂志文章abstract：:With multiple divisions in culture, normal diploid cells suffer a loss of growth potential that leads to replicative senescence and a finite replicative capacity. Using quantitative RT-PCR, we have monitored mRNA expression levels of c-fos, c-jun, JunB, c-myc, p53, H-ras, and histone H4 during the replicative senescen...
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更新日期：1986-12-01 00:00:00
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pub_type： 杂志文章,评审
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journal_title：Experimental cell research
pub_type： 杂志文章
doi：10.1006/excr.1994.1020
更新日期：1994-01-01 00:00:00
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pub_type： 杂志文章
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更新日期：1983-07-01 00:00:00
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