Summer Research Description: Plasminogen activator inhibitor-1 (PAI-1), a glycoprotein, inhibits the degradation of extracellular matrix through the plasminogen/plasmin pathway. A systemic PAI-1 knockout protects renal fibrosis induced by unilateral ureteral obstruction (UUO). Several kinds of cell secrete PAI-1, and PAI-1 also has direct cell regulation through the vitronectin/upAR pathway. By crossing tenascin C Cre mice (TNC-Cre) and PAI-1loxP/loxP mice, we found that knockdown of PAI-1 in fibroblasts is enough to reduce interstitial fibrosis in UUO. However, this is accompanied with more F4/80+ cell infiltration. The aim of this study is to investigate the subclasses of these F4/80+ cells, since both dendritic cells and macrophages express F4/80, and macrophage has both M1 and M2 subclasses with different functions. We will compare TNC-Cre/ PAI-1loxP/loxP mice with PAI-1loxP/loxP mice at day 10 after UUO. The ratio of CD11c to F4/80 will be detected by flow cytometry. F4/80+ cells will be sorted and M1 and M2 markers will be analyzed by real time PCR.