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Am J Physiol Renal Physiol (December 10, 2002). doi:10.1152/ajprenal.00343.2002
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Articles in PresS, published online ahead of print December 10, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00343.2002
Submitted on September 24, 2002
Accepted on December 3, 2002

CNP gene expression is activated by Wnt signaling and correlates with Wnt4 expression during renal injury

Kameswaran Surendran1 and Theodore C. Simon2*

1 Department of Biology and Biomedical Sciences, Washington University, St. Louis, MO, USA; Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA
2 Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: simon_t{at}kids.wustl.edu.

C-type natriuretic peptide (CNP) regulates salt excretion, vascular tone, and fibroblast proliferation and activation. CNP inhibits fibroblast activation in vitro and fibrosis in vivo, but endogenous CNP gene (Nppc) expression during tissue fibrosis has not been reported. We determined that Nppc is induced in renal tubular epithelia and then in interstitial myofibroblasts following unilateral ureteral obstruction (UUO). Induction of Nppc occurred in identical cell populations to those in which Wnt4 is induced following renal injury. In addition, Nppc was activated in Wnt4-expressing cells during nephrogenesis. Wnt signaling components {beta}-catenin and TCF/LEF transcription factors specifically bound to cognate elements in the Nppc proximal promoter. Wnt-4, {beta}-catenin, and LEF-1 activated an Nppc transgene in cultured cells, and transgene activation by LEF-1 was dependent on the presence of intact cognate elements. These findings suggest that Wnt-4 stimulates Nppc in a TCF/LEF-dependent manner following renal injury, and thus may contribute to limiting renal fibrosis.




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