STAT6 deficiency inhibits tubulointerstitial fibrosis in obstructive nephropathy.

Kazunori Yukawa, Masanori Kishino, Mikako Goda, Xiang Ming Liang, Akihiko Kimura, Tetsuji Tanaka, Tao Bai, Kyoko Owada-Makabe, Yuji Tsubota, Takashi Ueyama, Masakazu Ichinose, Masanobu Maeda, Kiyoshi Takeda, Shizuo Akira

研究成果: Article査読

17 被引用数 (Scopus)

抄録

To elucidate the contribution of signal transducer and activator of transcription (STAT) 6 to the pathophysiology of chronic renal injury, STAT6-/- mice were subjected to unilateral ureteral ligation together with wild-type control mice. STAT6-/- kidneys had more apoptotic cells and a greater influx of F4/80-positive cells than wild-type kidneys following ureteral obstruction. There was a much larger alpha-smooth muscle actin-positive area in STAT6-/- kidneys than in wild-type kidneys after ureteral ligation. However, renal fibrosis, as quantified by Masson-Trichrome staining, was not significantly exaggerated in STAT6-/- kidneys compared with wild-type kidneys. The accumulation of collagen I was significantly less in STAT6-/- kidneys than in wild-type kidneys. These observations indicate that the STAT6 signal transduction pathway exerts a protective role on renal cell apoptosis in chronic obstructive uropathy. Our findings also suggest that the STAT6 pathway may have a promotive effect on renal fibrosis by activating collagen synthesis following ureteral obstruction.

本文言語English
ページ(範囲)225-230
ページ数6
ジャーナルInternational journal of molecular medicine
15
2
DOI
出版ステータスPublished - 2005 2月

ASJC Scopus subject areas

  • 遺伝学

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