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Am J Physiol Renal Physiol 284: F653-F662, 2003. First published December 10, 2002; doi:10.1152/ajprenal.00343.2002
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Vol. 284, Issue 4, F653-F662, April 2003

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

Kameswaran Surendran1,2 and Theodore C. Simon1,3

1 Department of Pediatrics, 3 Department of Molecular Biology and Pharmacology, and 2 Division of Biology and Biomedical Sciences, Washington University School of Medicine, St. Louis, Missouri 63110

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 after unilateral ureteral obstruction (UUO). Induction of Nppc occurred in identical cell populations to those in which Wnt4 is induced after renal injury. In addition, Nppc was activated in Wnt4-expressing cells during nephrogenesis. Wnt signaling components beta -catenin and T cell factor/lymphoid enhancer binding factor (TCF/LEF) 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 Wnt-4 and 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 after renal injury and thus may contribute to limiting renal fibrosis.

myofibroblast; nephrogenesis; tubulointerstitial fibrosis; C-type natriuretic peptide


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