scholarly journals Exogenous Nitric Oxide Stimulates Cell Proliferation via Activation of a Mitogen-Activated Protein Kinase Pathway in Ovine Fetoplacental Artery Endothelial Cells1

2006 ◽  
Vol 74 (2) ◽  
pp. 375-382 ◽  
Author(s):  
Jing Zheng ◽  
YunXia Wen ◽  
Jason L. Austin ◽  
Dong-bao Chen
1998 ◽  
Vol 12 (2) ◽  
pp. 172-180 ◽  
Author(s):  
Masayoshi Shichiri ◽  
John M. Sedivy ◽  
Fumiaki Marumo ◽  
Yukio Hirata

Abstract 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 ETA 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 ETA receptor and the mitogen-activated protein kinase pathway.


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