17-ß-estradiol Decreases Neutrophil Superoxide Production through Rac1.
Exp Clin Endocrinol Diabetes
; 124(10): 588-592, 2016 Nov.
Article
em En
| MEDLINE
| ID: mdl-27437916
ABSTRACT
Neutrophil granulocytes form the biggest free radical producing system of the human body. The importance of this system in atherosclerotic plaque formation and other free radical mediated disorders is confirmed by both in vivo and in vitro studies. Estrogen's effect on free radical production involves multiple estrogen receptors and occurs both on transcriptional and on protein phosphorylational level. Estrogen decreases the superoxide production of neutrophil granulocytes in such a short time frame it is unlikely to be mediated by transcription regulation. We investigated the underlying mechanism through which the mentioned estrogen effect takes place using an immunabsorption-based method. Phosphorylation data of 43 different messenger proteins were used for pathway analysis. The newly identified pathway involved largely second messengers from previously described non-genomic estrogen effects and affected superoxide production via Rac1 - an important regulator of free radical production and chemotaxis. Selective inhibition of the participating second messengers altered superoxide production in the predicted direction confirming that this pathway is at least partly responsible for the effect of 17-ß-estradiol on chemoattractant induced superoxide production.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Superóxidos
/
Proteínas rac1 de Ligação ao GTP
/
Estradiol
/
Neutrófilos
Limite:
Adult
/
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Revista:
Exp Clin Endocrinol Diabetes
Assunto da revista:
ENDOCRINOLOGIA
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Hungria