| Literature DB >> 21281789 |
Noritoshi Kato1, Tomoki Kosugi, Waichi Sato, Takuji Ishimoto, Hiroshi Kojima, Yuka Sato, Kazuma Sakamoto, Shoichi Maruyama, Yukio Yuzawa, Seiichi Matsuo, Kenji Kadomatsu.
Abstract
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 β. Furthermore, Bsg(-/-) embryonic fibro blasts produced less hyaluronan and α-smooth muscle actin after transforming growth factor β 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.Entities:
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Year: 2011 PMID： 21281789 PMCID： PMC3069835 DOI： 10.1016/j.ajpath.2010.10.009
Source DB: PubMed Journal: Am J Pathol ISSN： 0002-9440 Impact factor: 4.307