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J Am Soc Nephrol 12:241-251, 2001
© 2001 American Society of Nephrology

Expression and Regulation of Estrogen Receptors in Mesangial Cells: Influence on Matrix Metalloproteinase-9

MYLENE POTIER*, SHARON J. ELLIOT*,{dagger}, IVAN TACK*, OLIVER LENZ*, GARY E. STRIKER*,{dagger},{ddagger}, LILIANE J. STRIKER*,{ddagger} and MICHAEL KARL*,{dagger},{ddagger}

* Renal Cell Biology Laboratory, Division of Nephrology, University of Miami School of Medicine, Miami, Florida.
{dagger} Division of Endocrinology, Diabetes and Metabolism, University of Miami School of Medicine, Miami, Florida.
{ddagger} Vascular Biology Institute, University of Miami School of Medicine, Miami, Florida.

Correspondence to Dr. Michael Karl, University of Miami School of Medicine, P.O. Box 016960 (R126), Miami, FL 33101. Phone: 305-243-2811; Fax: 305-243-2810; E-mail: mkarl{at}med.miami.edu

Abstract. Diabetic glomerulosclerosis is characterized by the accumulation of extracellular matrix (ECM) in the mesangium. Estrogens seem to retard whereas estrogen deficiency seems to accelerate progressive glomerulosclerosis. Thus, mesangial cells (MC) may be a target for estrogens. Estrogen action is mediated via estrogen receptor (ER) subtypes ER{alpha} and ERß. Both ER subtypes were expressed in human and mouse MC. Using an estrogen-responsive reporter construct in transfection assays, it also was demonstrated that the nuclear ER were transcriptionally active. In the presence of 17ß-estradiol (E2; 10-10 to 10-8 M), there was a progressive increase in the mRNA levels of both ER{alpha} (approximately 1.8-fold and approximately 2.7-fold after 24 and 72 h, respectively) and ERß (approximately 1.3-fold and approximately 2.2-fold after 24 and 72 h, respectively). ER{alpha} protein levels increased approximately 2.5-fold after 24 h (10-10 M, E2) and up to approximately 5.4-fold after 72 h (10-9 M, E2). ERß protein levels increased approximately 2.1-fold in the presence of E2 (10-9 M) after 24 h. Thus, estrogens positively regulate the expression of the ER subtypes, thereby maintaining or increasing MC responsiveness to estrogens. Because diabetic glomerulosclerosis may be due partly to a decrease in ECM degradation, the effects of estrogens on matrix metalloproteinases (MMP) were studied. It was found that E2 (10-10 to 10-8 M) increased both MMP-9 mRNA and MMP-9 activity in MC. This may be an important mechanism by which estrogens influence ECM turnover and protect against progression of diabetic glomerulosclerosis.




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