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Exp Clin Endocrinol Diabetes 2016; 124(10): 588-592
DOI: 10.1055/s-0042-105556
Article
© Georg Thieme Verlag KG Stuttgart · New York

17-β-estradiol Decreases Neutrophil Superoxide Production through Rac1

I. Marczell
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
,
A. Hrabak
2   Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Tűzoltó u. 37-47., H-1094 Budapest, Hungary
,
G. Nyiro
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
3   Office for Research Groups Attached to Universities and Other Institutions of the Hungarian Academy of Sciences, Molecular Medicine Research Group; H-1088, Budapest, Szentkirályi str. 46. Hungary
,
A. Patocs
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
4   Hungarian Academy of Sciences, Lendulet 2013 Research Group
,
J. Stark
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
,
E. Dinya
5   Faculty of Health and Public Services, Institute of Health Informatics Development and Further Training, Semmelweis University, Ulloi ut 78/b, Budapest, Hungary
,
Z. Kukor
3   Office for Research Groups Attached to Universities and Other Institutions of the Hungarian Academy of Sciences, Molecular Medicine Research Group; H-1088, Budapest, Szentkirályi str. 46. Hungary
,
S. Toth
6   Department of Genetics, Cell- and Immunobiology, Nagyvárad tér 4., H-1089 Budapest, Hungary
,
Z. S. Tulassay
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
,
K. Racz
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
,
G. Bekesi
1   2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
› Author Affiliations
Further Information

Publication History

received 01 February 2016
first decision 21 March 2016

accepted 24 March 2016

Publication Date:
20 July 2016 (online)

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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-β-estradiol on chemoattractant induced superoxide production.

Key words

estrogen receptor - estrogens - protein kinases
 

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