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(American Journal of Pathology. 2002;160:1877-1885.)
© 2002 American Society for Investigative Pathology

Regular Articles

Estrogen-Related Abnormalities in Glomerulosclerosis-Prone Mice

Reduced Mesangial Cell Estrogen Receptor Expression and Prosclerotic Response to Estrogens

Mylène Potier, Michael Karl, Feng Zheng, Sharon J. Elliot, Gary E. Striker and Liliane J. Striker

From the Vascular Biology Institute, Department of Medicine, University of Miami School of Medicine, Miami, Florida

The development and progression of glomerulosclerosis (GS) is determined by the genetic background. The incidence of end-stage renal disease is increased in postmenopausal women, suggesting that estrogen deficiency may play a role in the accumulation of extracellular matrix by mesangial cells (MCs), which are primarily responsible for the synthesis and degradation of this matrix. Using mouse models that are prone or resistant to the development of GS, we compared the expression of estrogen receptor (ER)-{alpha} and ER-ß subtypes in GS-prone and GS-resistant glomeruli and isolated MCs, and examined the effects of estrogens on ER, collagen, and matrix metalloproteinase (MMP) expression in MCs. Glomeruli and MCs from GS-prone mice had decreased expression of ER-{alpha} and ER-ß subtypes and ER transcriptional activity was also decreased in their MCs. Importantly, although 17ß-estradiol treatment resulted in decreased collagen accumulation and increased MMP-9 expression and activity in MCs from GS-resistant mice, there was, paradoxically, no effect on collagen accumulation and decreased MMP-9 expression and activity in MCs from GS-prone mice. Thus, GS susceptibility is associated with diminished ER expression in MCs. The renal protective effects of estrogens, including decreased collagen accumulation and increased MMP-9 expression, seem to be blunted in GS-prone MCs.




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