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Am J Physiol Renal Physiol (May 17, 2005). doi:10.1152/ajprenal.00065.2005
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Submitted on February 15, 2005
Accepted on May 15, 2005

SMP-534 inhibits TGF-{beta} induced ECM production in fibroblast cells and reduces mesangial matrix accumulation in experimental glomerulonephritis

Eiji Sugaru1, Mutsuko Sakai1, Kazuhiko Horigome2, Teruhisa Tokunaga3, Makoto Kitoh3, W. Ewan Hume3, Ryu Nagata3, Tsutomu Nakagawa1, and Mutsuo Taiji1*

1 Discovery Research Laboratories I, Sumitomo Pharmaceuticals Research Division, Osaka, Osaka, Japan
2 Genomic Research Laboratories, Sumitomo Pharmaceuticals Research Division, Osaka, Osaka, Japan
3 Chemical Research Laboratories, Sumitomo Pharmaceuticals Research Division, Osaka, Osaka, Japan

* To whom correspondence should be addressed. E-mail: taiji{at}sumitomopharm.co.jp.

Transforming growth factor-{beta} (TGF-{beta}) is a potent fibrotic factor responsible for the synthesis of extracellular matrix (ECM) and is implicated as the major determinant in pathogenesis of chronic fibroses, including kidney. The novel small compound, SMP-534, reduced ECM production induced by TGF-{beta} in fibroblast cells. SMP-534 inhibited TGF-{beta}-induced p38 mitogen activated protein kinase (p38) activation but did not inhibit epidermal growth factor (EGF)-induced extracellular signal-related kinase (ERK) activation. We also found that oral administration of SMP-534 dose-dependently lowered hydroxyproline contents in the cortical region of the kidney in rat anti-Thy-1 nephritis models. In periodic acid-Schiff staining of kidney sections, ECM accumulation was reduced by SMP-534 treatment. These data indicate that SMP-534 has potential in therapy for fibrotic diseases, including nephropathy.




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