| First Author | Zhou D | Year | 2013 |
| Journal | Sci Rep | Volume | 3 |
| Pages | 1878 | PubMed ID | 23698793 |
| Mgi Jnum | J:207805 | Mgi Id | MGI:5559656 |
| Doi | 10.1038/srep01878 | Citation | Zhou D, et al. (2013) Kidney tubular beta-catenin signaling controls interstitial fibroblast fate via epithelial-mesenchymal communication. Sci Rep 3:1878 |
| abstractText | Activation of beta-catenin, the principal mediator of canonical Wnt signaling, is a common pathologic finding in a wide variety of chronic kidney diseases (CKD). While beta-catenin is induced predominantly in renal tubular epithelium in CKD, surprisingly, depletion of tubular beta-catenin had little effect on the severity of renal fibrosis. Interestingly, less apoptosis was detected in interstitial fibroblasts in knockout mice, which was accompanied by a decreased expression of Bax and Fas ligand (FasL). Tubule-specific knockout of beta-catenin diminished renal induction of matrix metalloproteinase (MMP-7), which induced FasL expression in interstitial fibroblasts and potentiated fibroblast apoptosis in vitro. These results demonstrate that loss of tubular beta-catenin resulted in enhanced interstitial fibroblast survival due to decreased MMP-7 expression. Our studies uncover a novel role of the tubular beta-catenin/MMP-7 axis in controlling the fate of interstitial fibroblasts via epithelial-mesenchymal communication. |
