| First Author | Kato N | Year | 2011 |
| Journal | Am J Pathol | Volume | 178 |
| Issue | 2 | Pages | 572-9 |
| PubMed ID | 21281789 | Mgi Jnum | J:169085 |
| Mgi Id | MGI:4939838 | Doi | 10.1016/j.ajpath.2010.10.009 |
| Citation | Kato N, et al. (2011) Basigin/CD147 promotes renal fibrosis after unilateral ureteral obstruction. Am J Pathol 178(2):572-9 |
| abstractText | Regardless of their primary causes, progressive renal fibrosis and tubular atrophy are the main predictors of progression to end-stage renal disease. Basigin/CD147 is a multifunctional molecule-it induces matrix metalloproteinases and hyaluronan, for example-and has been implicated in organ fibrosis. However, the relationship between basigin and organ fibrosis has been poorly studied. We investigated basigin's role in renal fibrosis using a unilateral ureteral obstruction model. Basigin-deficient mice (Bsg(-/-)) demonstrated significantly less fibrosis after surgery than Bsg(+/+) mice. Fewer macrophages had infiltrated in Bsg(-/-) kidneys. Consistent with these in vivo data, primary cultured tubular epithelial cells from Bsg(-/-) mice produced less matrix metalloproteinase and exhibited less motility on stimulation with transforming growth factor beta. Furthermore, Bsg(-/-) embryonic fibro blasts produced less hyaluronan and alpha-smooth muscle actin after transforming growth factor beta stimulation. Together, these results demonstrate for the first time that basigin is a key regulator of renal fibrosis. Basigin could be a candidate target molecule for the prevention of organ fibrosis. |
