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Originally published In Press as doi:10.1074/jbc.M106670200 on January 2, 2002

J. Biol. Chem., Vol. 277, Issue 11, 9387-9394, March 15, 2002
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17beta -Estradiol Modulates Mechanical Strain-induced MAPK Activation in Mesangial Cells*

Joan KrepinskyDagger §, Alistair J. Ingram||, Leighton JamesDagger , Hao LyDagger , Kerri Thai, Daniel C. CattranDagger , Judith A. MillerDagger , and James W. ScholeyDagger **

From the Dagger  Department of Medicine, University of Toronto, Toronto, Ontario M5G 2C4, Canada and the  Department of Medicine, McMaster University, Hamilton, Ontario L8N 1Y2, Canada

Gender is an important determinant of clinical outcome across a broad spectrum of kidney diseases, but the mechanism(s) responsible for the protective effect of female gender have not been fully elucidated. Remnant kidney glomerular injury is limited in female rats compared with male rats despite similar elevations in glomerular capillary pressure. In vitro, mechanical strain leads to the activation of p44/42 mitogen-activated kinase (p44/42 MAPK) and Jun N-terminal kinase/stress-activated protein kinase (SAPK) in glomerular mesangial cells (MC). Accordingly, we studied the effect of 17beta -estradiol on mechanical strain-induced signal transduction in MC. Exposure of MC to mechanical strain increased p44/42 MAPK activation (3-fold) and SAPK activation (2.5-fold), and kinase activation was inhibited by pretreatment with 17beta -estradiol (10-8 to 10-11 M) for 24 h in a dose-dependent manner. Mechanical strain-induced nuclear translocation of p44/42 MAPK and SAPK and nuclear protein binding to AP-1 were also attenuated by 17beta -estradiol. The inhibitory effects of 17beta -estradiol were not reproduced by the cell-impermeable estrogen, BSA/17beta -estradiol, nor did preincubation with 17beta -estradiol lead to actin cytoskeleton disassembly or impaired stress fiber formation. However, 17beta -estradiol did increase base-line levels of the dual specificity phosphatase MKP-1. The inhibitory effects of 17beta -estradiol on p44/42 MAPK activation and SAPK activation, translocation, and AP-1 binding were all abrogated by the estrogen receptor antagonist, ICI-182,780. We conclude that attenuation of mechanical strain-induced MAPK activation by 17beta -estradiol is dependent on intracellular estrogen receptor. The attenuation of stretch-induced kinase activation may be due, at least in part, to an effect of 17beta -estradiol on MKP-1 expression. Together, these findings add insight into the protective effect of gender on renal disease progression.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by a research fellowship from Bristol-Myers-Squibb (Canada). To whom correspondence should be addressed: 13 EN-243, Toronto General Hospital, University Health Network, 200 Elizabeth St., Toronto, Ontario MUG 2C4, Canada. Tel.: 416-340-5093; Fax: 416-340-0029; E-mail: joan.krepinsky@utoronto.ca.

|| Supported by research funding from the Kidney Foundation of Canada.

** Supported by research funding from the Canadian Institutes of Health Research.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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