Tissue-specific deletion of Crry from mouse proximal tubular epithelial cells increases susceptibility to renal ischemia-reperfusion injury.

ABSTRACT: The murine cell surface protein Crry (complement receptor 1-related protein/gene y) is a key complement regulator with similar activities to human membrane cofactor protein (MCP) and decay-accelerating factor. MCP has a critical role in preventing complement-mediated tissue injury and its mutation has been implicated in several human kidney diseases. The study of Crry in mice has relevance to understanding MCP activity in human diseases; however, such efforts have been hampered by the embryonic lethality phenotype of Crry gene knockout. Here we used a conditional gene-targeting approach and deleted Crry from the mouse proximal tubular epithelial cells where Crry is prominently expressed. Absence of Crry from proximal tubular epithelial cells resulted in spontaneous C3 deposition on the bas

SUBMITTER: Miao J 

PROVIDER: S-EPMC4182132 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature