17-β-estradiol Decreases Neutrophil Superoxide Production through Rac1

I. Marczell; A. Hrabak; G. Nyiro; A. Patocs; J. Stark; E. Dinya; Z. Kukor; S. Toth; Z. S. Tulassay; K. Racz; G. Bekesi

doi:10.1055/s-0042-105556

Experimental and Clinical Endocrinology & Diabetes, Inhaltsverzeichnis

Exp Clin Endocrinol Diabetes 2016; 124(10): 588-592
DOI: 10.1055/s-0042-105556

Article

17-β-estradiol Decreases Neutrophil Superoxide Production through Rac1

Authors

I. Marczell

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
A. Hrabak

²Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Tűzoltó u. 37-47., H-1094 Budapest, Hungary
G. Nyiro

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary

³Office 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

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary

⁴Hungarian Academy of Sciences, Lendulet 2013 Research Group
J. Stark

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
E. Dinya

⁵Faculty of Health and Public Services, Institute of Health Informatics Development and Further Training, Semmelweis University, Ulloi ut 78/b, Budapest, Hungary
Z. Kukor

³Office 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

⁶Department of Genetics, Cell- and Immunobiology, Nagyvárad tér 4., H-1089 Budapest, Hungary
Z. S. Tulassay

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
K. Racz

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary
G. Bekesi

¹2nd Department of Medicine Semmelweis University; Szentkirályi utca 46., H-1088 Budapest, Hungary

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

Volltext

Referenzen

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