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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Sci+Rep 2014 ; 4 (ä): ä Nephropedia Template TP
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?2AP mediated myofibroblast formation and the development of renal fibrosis in unilateral ureteral obstruction #MMPMID25095732
Kanno Y; Kawashita E; Kokado A; Kuretake H; Ikeda K; Okada K; Seishima M; Ueshima S; Matsuo O; Matsuno H
Sci Rep 2014[]; 4 (ä): ä PMID25095732show ga
Renal fibrosis is the final common pathway of a wide variety of chronic kidney diseases. Myofibroblast formation via the differentiation of from tissue-resident fibroblasts and bone marrow-derived mesenchymal stem cells (MSCs), and epithelial-to-mesenchymal transition (EMT) is known to play a pivotal role in the development of renal fibrosis. However, the detailed mechanisms underlying this disorder remain unclear. We herein investigated the role of alpha 2-antiplasmin (?2AP) in myofibroblast formation and the development of renal fibrosis. We observed the development of renal fibrosis using unilateral ureteral obstruction (UUO). ?2AP had accumulated in the UUO-induced obstructed kidneys and ?2AP deficiency attenuated UUO-induced renal fibrosis in mice. The degree of myofibroblast formation in the obstructed kidneys of ?2AP?/? mice was less than that in ?2AP+/+ mice. In vitro, ?2AP induced myofibroblast formation in renal tubular epithelial cells (RTECs), renal fibrosblasts, and bone marrow-derived mesenchymal stem cells (MSCs). ?2AP also induced the production of TGF-?, which is known to be a key regulator of myofibroblast formation and fibrosis. ?2AP-induced the TGF-? production was significantly reduced by SP600125, c-Jun N-terminal kinase (JNK) specific inhibitor. Our findings suggest that ?2AP induces myofibroblast formation in the obstructed kidneys, and mediates the development of renal fibrosis.