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- W583398998 abstract "Nitric oxide (NO) has been shown to antagonize the mitogenic and hypertrophic responses of growth factors and vasoactive peptides such as endothelin-1 (ET-1) inVSMCs. However, the mechanism by which NO exerts its anti-mitogenic and anti-hypertrophic effect remains unknown. Therefore, the aim of this study was to determine if NO generation would modify ET-1-induced signaling pathways involved in cellular growth, proliferation and hypertrophy in VSMC. Treatment of VSMCs with SNAP, a NO donor, attenuated the ET-1-enhanced phosphorylation of several key components of growth promoting and hypertrophic signaling pathways such as ERK1/2, PKB and Pyk2. Since, NO mediates its effect principally through a cyclic GMP/soluble guanylate cyclase (GC) pathway, we investigated the role of these molecules in NO action. 8-Br-cGMP, a non-metabolizable and cell permeable analogue of cGMP, exhibited a similar effect as SNAP and inhibited ET-1-induced ERK1/2, PKB and Pyk2 phosphorylation. Furthermore, ODQ, an inhibitor of soluble GC activity, reversed the inhibitory effect of NO on ET-1-induced responses. SNAP also decreased the protein synthesis induced by ET-1. Taken together, these data demonstrate that NO, in a cGMP-dependent manner, attenuated ET-1-induced phosphorylation of ERK1/2, PKB and Pyk2 and also antagonized the hypertrophic effects of ET-1. It may be suggested that NO-induced generation of cyclic GMP contributes to the inhibition of ET-1-induced mitogenic and hypertrophic response s in VSMCs. (Supported by a grant from Canadian Institutes of Health Research)" @default.
- W583398998 created "2016-06-24" @default.
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- W583398998 date "2006-03-01" @default.
- W583398998 modified "2023-10-16" @default.
- W583398998 title "Cyclic GMP‐mediates NO‐induced attenuation of endothelin‐1 signaling and hypertrophic response in vascular smooth muscle cells (VSMC)." @default.
- W583398998 doi "https://doi.org/10.1096/fasebj.20.4.a104-d" @default.
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