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1 Department of Medicine, University of Minnesota Health Service Center, Minneapolis, MN, USA
* To whom correspondence should be addressed. E-mail: bache001{at}tc.umn.edu.
Previously we found that IL-1
-activated inducible nitric oxide (NO) synthase (iNOS) expression and NO production can trigger cardiac fibroblast (CFb) apoptosis. Here, we provide evidence that angiotensin II (Ang II) significantly attenuated IL-1-induced iNOS expression and NO production in CFbs while simultaneously decreasing apoptotic frequency. The anti-apoptotic effect of Ang II was abolished when cells were pretreated with the specific Ang II type I receptor (AT1) antagonist losartan, but not by the AT2 antagonist DP123319. Furthermore, Ang II also protected CFbs from apoptosis induced by the NO donor DETA NONOate and this effect was associated with phosphorylation of Akt/PKB at Serine 473. The effects of Ang II on Akt phosphorylation and NO donor-induced CFb apoptosis were abrogated when cells were pre-incubated with the specific PI3-kinase inhibitors wortmannin or LY294002. These data demonstrate that Ang II protection of CFbs from IL-1-induced apoptosis is associated with down regulation of iNOS expression and requires an intact PI3K-Akt survival signal pathway. The findings suggest that Ang II and NO may play a role in regulating the cell population size by their countervailing influences on cardiac fibroblast viability.
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