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Am J Physiol Renal Physiol (January 8, 2002). doi:10.1152/ajprenal.00240.2001
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Articles in PresS, published online ahead of print January 8, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00240.2001
Submitted on August 1, 2001
Accepted on January 3, 2002

Angiotensin II Induces Apoptosis of Rat Glomerular Epithelial Cells

Guohua Ding1, Krishna Reddy2, Aditi A Kapasi2, Nicholas Franki2, Nora Gibbons2, Balakuntalam S Kasinath3, and Pravin C Singhal2*

1 Department of Medicine, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medice, New Hyde Park, New York, USA; Department of Medicine, Medical College of Wuhan University, Renmin Hospital, Wuhan, Hubei, China
2 Department of Medicine, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medice, New Hyde Park, New York, USA
3 Department of Medicine, University of Texas Health Science Center, San Antonio, Texas, USA

* To whom correspondence should be addressed. E-mail: singhal{at}lij.edu.

Angiotensin II (ANG II) has been shown to modulate kidney cell growth and contribute to the pathobiology of glomerulosclerosis. Glomerular visceral epithelial cell (GEC) injury or loss is considered to play a pivotal role in the initiation and progression of glomerulosclerosis. In the present study, we investigated the effect of ANG II on GEC apoptosis. Rat GEC were incubated with increasing doses of ANG II for variable time periods. Apoptosis was evaluated by cell nucleus staining and DNA fragmentation assay. ANG II induced GEC apoptosis in a dose- and time-dependent manner. The pro-apoptotic effect was attenuated by the AT1 receptor antagonist losartan or the AT2 receptor antagonist PD123319, and completely blocked by the incubation with the combined antagonists. Moreover, ANG II stimulated TGF-ß1 production as measured by ELISA. GEC exposed to TGF-ß1 demonstrated a dose- and time-dependent increase in apoptosis. ANG II-induced apoptosis was significantly inhibited by addition of anti-TGF-ß1 antibody. ANG II also up-regulated the expression of Fas, FasL, and Bax and down-regulated the expression of Bcl-2 in GEC. These studies suggest that ANG II induces GEC apoptosis by a mechanism involving TGF-ß1 expression which may, importantly, contribute to the pathogenesis of glomerulosclerosis.




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