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Loss of the BMP antagonist USAG-1 ameliorates disease in a mouse model of the progressive hereditary kidney disease Alport syndrome
http://hdl.handle.net/2297/27064
http://hdl.handle.net/2297/27064892de070-f42a-42bd-a139-957481e517d3
名前 / ファイル | ライセンス | アクション |
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ME-PR-SAKURAI-T-768.pdf (4.7 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-03 | |||||
タイトル | ||||||
タイトル | Loss of the BMP antagonist USAG-1 ameliorates disease in a mouse model of the progressive hereditary kidney disease Alport syndrome | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Tanaka, Mari
× Tanaka, Mari× Asada, Misako× Higashi, Atsuko Y.× Nakamura, Jin× Oguchi, Akiko× Tomita, Mayumi× Yamada, Sachiko× Asada, Nariaki× Takase, Masayuki× Okuda, Tomohiko× Kawachi, Hiroshi× Economides, Aris N.× Robertson, Elizabeth× Takahashi, Satoru× Sakurai, Takeshi× Goldschmeding, Roel× Muso, Eri× Fukatsu, Atsushi× Kita, Toru× Yanagita, Motoko |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
Journal of Clinical Investigation 巻 120, 号 3, p. 768-777, 発行日 2010-03-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9738 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00695520 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1172/JCI39569 | |||||
出版者 | ||||||
出版者 | American Society for Clinical Investigation | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The glomerular basement membrane (GBM) is a key component of the filtering unit in the kidney. Mutations involving any of the collagen IV genes (COL4A3, COL4A4, and COL4A5) affect GBM assembly and cause Alport syndrome, a progressive hereditary kidney disease with no definitive therapy. Previously, we have demonstrated that the bone morphogenetic protein (BMP) antagonist uterine sensitization-associated gene-1 (USAG-1) negatively regulates the renoprotective action of BMP-7 in a mouse model of tubular injury during acute renal failure. Here, we investigated the role of USAG-1 in renal function in Col4a3 -/- mice, which model Alport syndrome. Ablation of Usag1 in Col4a3-/- mice led to substantial attenuation of disease progression, normalization of GBM ultrastructure, preservation of renal function, and extension of life span. Immunohistochemical analysis revealed that USAG-1 and BMP-7 colocalized in the macula densa in the distal tubules, lying in direct contact with glomerular mesangial cells. Furthermore, in cultured mesangial cells, BMP-7 attenuated and USAG-1 enhanced the expression of MMP-12, a protease that may contribute to GBM degradation. These data suggest that the pathogenetic role of USAG-1 in Col4a3-/- mice might involve crosstalk between kidney tubules and the glomerulus and that inhibition of USAG-1 may be a promising therapeutic approach for the treatment of Alport syndrome. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |