Endothelin-1 Is a Potent Survival Factor for c-Myc-Dependent Apoptosis
Author(s) -
Masayoshi Shichiri,
John M. Sedivy,
Fumiaki Marumo,
Yukio Hirata
Publication year - 1998
Publication title -
molecular endocrinology
Language(s) - English
Resource type - Journals
eISSN - 1944-9917
pISSN - 0888-8809
DOI - 10.1210/mend.12.2.0064
Subject(s) - biology , apoptosis , endothelin 1 , cancer research , microbiology and biotechnology , medicine , genetics , receptor
Many vertebrate cells are resistant to apoptotic stimuli, whose variety and the mechanisms involved are not fully understood. Endothelin-1 is an endothelium-derived vasoactive peptide that mediates many physiological functions, such as vasoconstriction and cell proliferation. Deregulated expression of c-Myc induces apoptosis in serum-deprived fibroblasts. Using a panel of isogenic fibroblast cell lines with differential c-myc expression levels, we demonstrate that low doses of endothelin-1 protect fibroblasts against serum deprivation-induced apoptosis, which occurs through a c-Myc-dependent process. The endothelin-1-induced cell survival was mediated by the ET(A) receptor and was not linked to the ability of endothelin-1 to induce cell proliferation. The survival function of endothelin-1 was abrogated by inhibiting the mitogen-activated protein kinase pathway. These results demonstrate a hitherto unappreciated role of endothelin-1 as a potent survival factor for c-Myc-dependent apoptosis, a process mediated by the ET(A) receptor and the mitogen-activated protein kinase pathway.
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