Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.

Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. It is also known that the lower risk of cardiovascular diseases in female is partially attributed to the protective effect of estrogen. The curr...

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Autores principales:	Hongzhu Li, Sarathi Mani, Wei Cao, Guangdong Yang, Christopher Lai, Lingyun Wu, Rui Wang
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b08f34aa797c4087be1edf7c5fc732d0
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spelling	oai:doaj.org-article:b08f34aa797c4087be1edf7c5fc732d02021-11-18T07:09:52ZInteraction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.1932-620310.1371/journal.pone.0041614https://doaj.org/article/b08f34aa797c4087be1edf7c5fc732d02012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22870237/?tool=EBIhttps://doaj.org/toc/1932-6203Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. It is also known that the lower risk of cardiovascular diseases in female is partially attributed to the protective effect of estrogen. The current study explores the interaction of H(2)S and estrogen on smooth muscle cell (SMC) growth. In the present study, we found that the proliferation of cultured vascular SMCs isolated from wild-type mice (WT-SMCs) was inhibited, but that from CSE gene knockout mice (CSE-KO-SMCs) increased, by estrogen treatments. The expression of estrogen receptor α (ERα), but not ERβ, was significantly decreased in CSE-KO-SMCs compared with that in WT-SMCs. Exogenously applied H(2)S markedly increased ERα but not ERβ expression. In addition, the inhibition of ER activation and knockdown of ERα expression in WT-SMCs or the overexpression of ERα in CSE-KO-SMCs reversed the respective effects of estrogen on cell proliferation. The expression of cyclin D1 was reduced in WT-SMCs but increased in CSE-KO-SMCs after estrogen treatments, which was reversed by knockdown of ERα in WT-SMCs or overexpression of ERα in CSE-KO-SMCs, respectively. The overexpression of cyclin D1 in WT-SMCs or knockdown of cyclin D1 expression in CSE-KO-SMCs reversed the effects of estrogen on cell proliferation. These results suggest that H(2)S mediates estrogen-inhibited proliferation of SMCs via selective activation of ERα/cyclin D1 pathways.Hongzhu LiSarathi ManiWei CaoGuangdong YangChristopher LaiLingyun WuRui WangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 8, p e41614 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hongzhu Li Sarathi Mani Wei Cao Guangdong Yang Christopher Lai Lingyun Wu Rui Wang Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
description	Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. It is also known that the lower risk of cardiovascular diseases in female is partially attributed to the protective effect of estrogen. The current study explores the interaction of H(2)S and estrogen on smooth muscle cell (SMC) growth. In the present study, we found that the proliferation of cultured vascular SMCs isolated from wild-type mice (WT-SMCs) was inhibited, but that from CSE gene knockout mice (CSE-KO-SMCs) increased, by estrogen treatments. The expression of estrogen receptor α (ERα), but not ERβ, was significantly decreased in CSE-KO-SMCs compared with that in WT-SMCs. Exogenously applied H(2)S markedly increased ERα but not ERβ expression. In addition, the inhibition of ER activation and knockdown of ERα expression in WT-SMCs or the overexpression of ERα in CSE-KO-SMCs reversed the respective effects of estrogen on cell proliferation. The expression of cyclin D1 was reduced in WT-SMCs but increased in CSE-KO-SMCs after estrogen treatments, which was reversed by knockdown of ERα in WT-SMCs or overexpression of ERα in CSE-KO-SMCs, respectively. The overexpression of cyclin D1 in WT-SMCs or knockdown of cyclin D1 expression in CSE-KO-SMCs reversed the effects of estrogen on cell proliferation. These results suggest that H(2)S mediates estrogen-inhibited proliferation of SMCs via selective activation of ERα/cyclin D1 pathways.
format	article
author	Hongzhu Li Sarathi Mani Wei Cao Guangdong Yang Christopher Lai Lingyun Wu Rui Wang
author_facet	Hongzhu Li Sarathi Mani Wei Cao Guangdong Yang Christopher Lai Lingyun Wu Rui Wang
author_sort	Hongzhu Li
title	Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
title_short	Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
title_full	Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
title_fullStr	Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
title_full_unstemmed	Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
title_sort	interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/b08f34aa797c4087be1edf7c5fc732d0
work_keys_str_mv	AT hongzhuli interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT sarathimani interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT weicao interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT guangdongyang interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT christopherlai interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT lingyunwu interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells AT ruiwang interactionofhydrogensulfideandestrogenontheproliferationofvascularsmoothmusclecells
_version_	1718423874774761472

Interaction of hydrogen sulfide and estrogen on the proliferation of vascular smooth muscle cells.

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