Gender differences in S-nitrosoglutathione reductase activity in the lung.

S-nitrosothiols have been implicated in the etiology of various pulmonary diseases. Many of these diseases display gender preferences in presentation or altered severity that occurs with puberty, the mechanism by which is unknown. Estrogen has been shown to influence the expression and activity of e...

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Autores principales:	Kathleen Brown-Steinke, Kimberly deRonde, Sean Yemen, Lisa A Palmer
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/aa0f7e00d8a44e00a46855f924fb882c
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spelling	oai:doaj.org-article:aa0f7e00d8a44e00a46855f924fb882c2021-11-18T07:36:46ZGender differences in S-nitrosoglutathione reductase activity in the lung.1932-620310.1371/journal.pone.0014007https://doaj.org/article/aa0f7e00d8a44e00a46855f924fb882c2010-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21103380/?tool=EBIhttps://doaj.org/toc/1932-6203S-nitrosothiols have been implicated in the etiology of various pulmonary diseases. Many of these diseases display gender preferences in presentation or altered severity that occurs with puberty, the mechanism by which is unknown. Estrogen has been shown to influence the expression and activity of endothelial nitric oxide synthase (eNOS) which is associated with increased S-nitrosothiol production. The effects of gender hormones on the expression and activity of the de-nitrosylating enzyme S-nitrosoglutathione reductase (GSNO-R) are undefined. This report evaluates the effects of gender hormones on the activity and expression of GSNO-R and its relationship to N-acetyl cysteine (NAC)-induced pulmonary hypertension (PH). GSNO-R activity was elevated in lung homogenates from female compared to male mice. Increased activity was not due to changes in GSNO-R expression, but correlated with GSNO-R S-nitrosylation: females were greater than males. The ability of GSNO-R to be activated by S-nitrosylation was confirmed by: 1) the ability of S-nitrosoglutathione (GSNO) to increase the activity of GSNO-R in murine pulmonary endothelial cells and 2) reduced activity of GSNO-R in lung homogenates from eNOS(-/-) mice. Gender differences in GSNO-R activity appear to explain the difference in the ability of NAC to induce PH: female and castrated male animals are protected from NAC-induced PH. Castration results in elevated GSNO-R activity that is similar to that seen in female animals. The data suggest that GSNO-R activity is modulated by both estrogens and androgens in conjunction with hormonal regulation of eNOS to maintain S-nitrosothiol homeostasis. Moreover, disruption of this eNOS-GSNO-R axis contributes to the development of PH.Kathleen Brown-SteinkeKimberly deRondeSean YemenLisa A PalmerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 11, p e14007 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kathleen Brown-Steinke Kimberly deRonde Sean Yemen Lisa A Palmer Gender differences in S-nitrosoglutathione reductase activity in the lung.
description	S-nitrosothiols have been implicated in the etiology of various pulmonary diseases. Many of these diseases display gender preferences in presentation or altered severity that occurs with puberty, the mechanism by which is unknown. Estrogen has been shown to influence the expression and activity of endothelial nitric oxide synthase (eNOS) which is associated with increased S-nitrosothiol production. The effects of gender hormones on the expression and activity of the de-nitrosylating enzyme S-nitrosoglutathione reductase (GSNO-R) are undefined. This report evaluates the effects of gender hormones on the activity and expression of GSNO-R and its relationship to N-acetyl cysteine (NAC)-induced pulmonary hypertension (PH). GSNO-R activity was elevated in lung homogenates from female compared to male mice. Increased activity was not due to changes in GSNO-R expression, but correlated with GSNO-R S-nitrosylation: females were greater than males. The ability of GSNO-R to be activated by S-nitrosylation was confirmed by: 1) the ability of S-nitrosoglutathione (GSNO) to increase the activity of GSNO-R in murine pulmonary endothelial cells and 2) reduced activity of GSNO-R in lung homogenates from eNOS(-/-) mice. Gender differences in GSNO-R activity appear to explain the difference in the ability of NAC to induce PH: female and castrated male animals are protected from NAC-induced PH. Castration results in elevated GSNO-R activity that is similar to that seen in female animals. The data suggest that GSNO-R activity is modulated by both estrogens and androgens in conjunction with hormonal regulation of eNOS to maintain S-nitrosothiol homeostasis. Moreover, disruption of this eNOS-GSNO-R axis contributes to the development of PH.
format	article
author	Kathleen Brown-Steinke Kimberly deRonde Sean Yemen Lisa A Palmer
author_facet	Kathleen Brown-Steinke Kimberly deRonde Sean Yemen Lisa A Palmer
author_sort	Kathleen Brown-Steinke
title	Gender differences in S-nitrosoglutathione reductase activity in the lung.
title_short	Gender differences in S-nitrosoglutathione reductase activity in the lung.
title_full	Gender differences in S-nitrosoglutathione reductase activity in the lung.
title_fullStr	Gender differences in S-nitrosoglutathione reductase activity in the lung.
title_full_unstemmed	Gender differences in S-nitrosoglutathione reductase activity in the lung.
title_sort	gender differences in s-nitrosoglutathione reductase activity in the lung.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/aa0f7e00d8a44e00a46855f924fb882c
work_keys_str_mv	AT kathleenbrownsteinke genderdifferencesinsnitrosoglutathionereductaseactivityinthelung AT kimberlyderonde genderdifferencesinsnitrosoglutathionereductaseactivityinthelung AT seanyemen genderdifferencesinsnitrosoglutathionereductaseactivityinthelung AT lisaapalmer genderdifferencesinsnitrosoglutathionereductaseactivityinthelung
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Gender differences in S-nitrosoglutathione reductase activity in the lung.

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