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Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.

Altaany Z, Yang G, Wang R - J. Cell. Mol. Med. (2013)

Bottom Line: Their interaction at different levels would have a profound impact on angiogenesis.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.Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.

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H2S-stimulated endothelial cell (EC) proliferation. (A) The effects of NaHS treatment on EC proliferation assessed using BrdU proliferation assay. n = 3, *P < 0.05 versus control. (B) The effects of cystathionine gamma-lyase (CSE) knockdown or overexpression on EC proliferation. n = 3, *P < 0.05 versus control. (C) The efficiency of endothelial NO synthase (eNOS) overexpression in ECs detected by Western blot, n = 3, *P < 0.05 versus Mock. (D) The effect of eNOS overexpression on EC proliferation. n = 3, *P < 0.05 versus Mock.
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fig06: H2S-stimulated endothelial cell (EC) proliferation. (A) The effects of NaHS treatment on EC proliferation assessed using BrdU proliferation assay. n = 3, *P < 0.05 versus control. (B) The effects of cystathionine gamma-lyase (CSE) knockdown or overexpression on EC proliferation. n = 3, *P < 0.05 versus control. (C) The efficiency of endothelial NO synthase (eNOS) overexpression in ECs detected by Western blot, n = 3, *P < 0.05 versus Mock. (D) The effect of eNOS overexpression on EC proliferation. n = 3, *P < 0.05 versus Mock.

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).


Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.

Altaany Z, Yang G, Wang R - J. Cell. Mol. Med. (2013)

H2S-stimulated endothelial cell (EC) proliferation. (A) The effects of NaHS treatment on EC proliferation assessed using BrdU proliferation assay. n = 3, *P < 0.05 versus control. (B) The effects of cystathionine gamma-lyase (CSE) knockdown or overexpression on EC proliferation. n = 3, *P < 0.05 versus control. (C) The efficiency of endothelial NO synthase (eNOS) overexpression in ECs detected by Western blot, n = 3, *P < 0.05 versus Mock. (D) The effect of eNOS overexpression on EC proliferation. n = 3, *P < 0.05 versus Mock.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3822893&req=5

fig06: H2S-stimulated endothelial cell (EC) proliferation. (A) The effects of NaHS treatment on EC proliferation assessed using BrdU proliferation assay. n = 3, *P < 0.05 versus control. (B) The effects of cystathionine gamma-lyase (CSE) knockdown or overexpression on EC proliferation. n = 3, *P < 0.05 versus control. (C) The efficiency of endothelial NO synthase (eNOS) overexpression in ECs detected by Western blot, n = 3, *P < 0.05 versus Mock. (D) The effect of eNOS overexpression on EC proliferation. n = 3, *P < 0.05 versus Mock.
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).

Bottom Line: Their interaction at different levels would have a profound impact on angiogenesis.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.Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.

Show MeSH