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The Orphan Nuclear Receptor SHP Attenuates Renal Fibrosis
DC Field | Value | Language |
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dc.contributor.author | Jung, Gwon-Soo | - |
dc.contributor.author | Kim, Mi-Kyung | - |
dc.contributor.author | Choe, Mi Sun | - |
dc.contributor.author | Lee, Kyeong-Min | - |
dc.contributor.author | Park, Young Joo | - |
dc.contributor.author | Lee, Ki-Up | - |
dc.contributor.author | Lee, In-Kyu | - |
dc.contributor.author | Park, Keun-Gyu | - |
dc.contributor.author | Choi, Hueng-Sik | - |
dc.contributor.author | Kim, Hye-Soon | - |
dc.date.accessioned | 2012-06-26T04:59:43Z | - |
dc.date.available | 2012-06-26T04:59:43Z | - |
dc.date.issued | 2009-10 | - |
dc.identifier.citation | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY; Vol.20 10; 2162-2170 | ko_KR |
dc.identifier.issn | 1046-6673 | - |
dc.identifier.uri | https://hdl.handle.net/10371/77425 | - |
dc.description.abstract | The accumulation of extracellular matrix proteins is a common feature of fibrotic kidney diseases. Accumulating evidence suggests that TGF-beta and plasminogen activator inhibitor type 1 (PAI-1) promote the development of renal fibrosis by stimulating the generation and inhibiting the removal of matrix proteins. The small heterodimer partner (SHP) represses PAI-1 expression in the liver by inhibiting TGF-beta signaling, but whether SHP inhibits renal fibrosis is unknown. Here, unilateral ureteral obstruction (UUO) markedly increased the expression of PAI-1, type I collagen, and fibronectin but decreased SHP gene expression. Moreover, in kidneys of SHP-/- mice, the expression of PAI-1, type I collagen, fibronectin and a-smooth muscle actin (alpha-SMA) were higher compared with those in kidneys of wild-type mice. In addition, loss of SHP accelerated renal fibrosis after UUO. Adenovirus-mediated overexpression of SHP in cultured rat mesangial cells and renal tubular epithelial cells inhibited TGF-beta-stimulated expression of PAI-1, type I collagen, and fibronectin. SHP inhibited TGF-beta- and Smad3-stimulated PAI-1 promoter activities as well as TGF-beta-stimulated binding of Smad3 to its consensus response element on the PAI-1 promoter. Similarly, in vivo, adenovirus-mediated overexpression of SHP in the kidney inhibited the expression of UUO-induced PAI-1, type I collagen, fibronectin, and alpha-SMA. In summary, SHP attenuates renal fibrosis in obstructive nephropathy, making its pathway a possible therapeutic target for chronic kidney disease. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | AMER SOC NEPHROLOGY | ko_KR |
dc.title | The Orphan Nuclear Receptor SHP Attenuates Renal Fibrosis | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 정권수 | - |
dc.contributor.AlternativeAuthor | 김미경 | - |
dc.contributor.AlternativeAuthor | 최미선 | - |
dc.contributor.AlternativeAuthor | 이경민 | - |
dc.contributor.AlternativeAuthor | 김혜순 | - |
dc.contributor.AlternativeAuthor | 박영주 | - |
dc.contributor.AlternativeAuthor | 최흥식 | - |
dc.contributor.AlternativeAuthor | 이기업 | - |
dc.contributor.AlternativeAuthor | 박근규 | - |
dc.contributor.AlternativeAuthor | 이인규 | - |
dc.identifier.doi | 10.1681/ASN.2008121232 | - |
dc.citation.journaltitle | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | - |
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