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Modulation by bradykinin and nitric oxide of angiotensin II-induced apoptosis in a vascular smooth muscle cell phenotype.

Abstract : There is evidence for a clinical benefit of ACE inhibitors or AT1 antagonists in cardiovascular diseases with deleterious smooth muscle cells (SMC) apoptosis. We have previously shown that angiotensin II (Ang II) induces a phenotype-dependent SMC apoptosis. We asked whether bradykinin (BK) and nitric oxide (NO) could modulate Ang II-induced SMC apoptosis. BK alone did not induce significant apoptosis in either spindle (Sp-SMC) or epithelioid (Ep-SMC) SMC phenotypes cultured in serum reduction, but phenotype-dependently, reduced cell proliferation. Pretreatment with BK partly impaired Ang II-induced reduction of Ep-SMC culture viability and partly prevented apoptotic features. Pretreatment with sodium nitroprusside completely prevented all Ang II-induced deleterious effects in Ep-SMC, i. e. reduction of culture viability, Annexin V binding, nuclear condensation and cell fragmentation. These findings indicate that the BK-NO system may phenotype-dependently modulate SMC survival and in particular may oppose, mostly by NO, Ang II-induction of apoptosis in the Ep-SMC phenotype.
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https://www.hal.inserm.fr/inserm-00408917
Contributor : Marie Francoise Simon <>
Submitted on : Tuesday, August 4, 2009 - 1:52:46 PM
Last modification on : Friday, January 10, 2020 - 9:09:08 PM

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Sandra Colie, Christiane Pecher, Jean-Pierre Girolami, Nelly Blaes. Modulation by bradykinin and nitric oxide of angiotensin II-induced apoptosis in a vascular smooth muscle cell phenotype.. International Immunopharmacology, Elsevier, 2008, 8 (2), pp.231-6. ⟨10.1016/j.intimp.2007.09.006⟩. ⟨inserm-00408917⟩

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