Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.
Bottom Line: H2 S had little effect on eNOS protein expression in ECs.LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.
Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.Show MeSH
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Mentions: NaHS significantly induced EC proliferation (Fig. 6A). To show the effect of endogenously produced H2S, CSE knockdown with a siRNA approach attenuated cell proliferation. The knockdown of CSE significantly attenuated the proliferation of EC by about 25% compared with the control group (Fig. 6B). We also found that CSE knockdown significantly decreased, but NaHS induced a similar and comparable increase, in the proliferation of primarily cultured mouse ECs (Figure S2). The CSE overexpression stimulated EC proliferation (Fig. 6B). Next, we study the effect of NO on proliferation. The overexpression of eNOS stimulated cell proliferation, which was strengthened by NaHS treatment (Fig. 6C and D).
Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.