Angiotensin II increases fibronectin and collagen I through the β-catenin dependent signaling in mouse collecting duct cells.

In this study we investigated whether AT1 receptor activation induces the expression of fibronectin and collagen I via the β-catenin pathway in mouse collecting duct cell line M-1. Ang II (10(-7) M) treatment in M-1 cells increased mRNA, protein levels of fibronectin and collagen I, the β-catenin target genes (cyclin D1 and c-myc), and the myofibroblast phenotype. These effects were prevented by candesartan, an AT1 receptor blocker. Inhibition of the β-catenin degradation with pyrvinium pamoate (pyr, 10(-9) M) prevented the Ang II-induced expression of fibronectin, collagen I, and β-catenin target genes. Ang II treatment promoted the accumulation of β-catenin protein in a time-dependent manner. Because phosphorylation of GSK-3β inhibits β-catenin degradation, we further evaluated the effects of Ang II and Ang II plus pyr on p-ser9-GSK-3β levels. Ang II-dependent upregulation of β-catenin protein levels were correlated with GSK-3β phosphorylation. These effects were prevented by pyrvinium pamoate. Our data indicate that in M-1 collecting duct cells, the β-catenin pathway mediates the stimulation of fibronectin and collagen I in response to AT1 receptor activation. PMID: 25411386 [PubMed - as supplied by publisher]
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research

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