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Am J Physiol Renal Physiol (October 1, 2002). doi:10.1152/ajprenal.00115.2002
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Articles in PresS, published online ahead of print October 1, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00115.2002
Submitted on March 25, 2002
Accepted on September 24, 2002

Bradykinin reduces growth factor-induced glomerular Erk1/2 phosphorylation

Eric Cellier1, Marilyne Mage1, Johan Duchene1, Christiane Pecher1, Rejean Couture2, Jean-Loup Bascands1, and Jean-Pierre Girolami1*

1 INSERM U388, IFR31, Institut Louis Bugnard, Toulouse, France
2 Department of physiology, Universite de Montreal, Montreal, Canada

* To whom correspondence should be addressed. E-mail: girolami{at}toulouse.inserm.fr.

Several experimental data report both mitogenic and antimitogenic effects of BK. To conciliate these apparent opposite effects, we hypothesized that, depending upon cell context activation, BK could reduce the mitogenic effect of growth factors. Therefore, we assessed in the present study the existence of a possible negative cross-talk between BK and potential pathogenic growth factors in freshly isolated rat glomeruli (IG). Next, we determined whether this cross talk could be pharmacologically recruited during ACE inhibition in the diabetic rat. In IG from normal rats, BK, via activation of the B2-kinin receptor (B2R), causes a transient stimulation of Erk1/2 phosphorylation, whereas it inhibits Erk1/2 phosphorylation induced by IGF-1, PDGF-BB, VEGF or bFGF. The reduction of growth factors-induced Erk1/2 phosphorylation is abolished by an inhibitor of tyrosine phosphatase. In glomeruli from diabetic rats, hyperglycemia increased the phosphorylation level of Erk-1/2 as well as oxidative stress. The reversal of these events by ACE inhibition is mediated via B2R activation. These observations are consistent with a potential therapeutic role of BK and B2R during glomerulosclerosis.




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