Deletion of TRPC3 or TRPC6 fails to attenuate the formation of inflammation and fibrosis in non-alcoholic steatohepatitis

Kazuhiro Nishiyama, Chiemi Toyama, Yuri Kato, Tomohiro Tanaka, Akiyuki Nishimura, Ryu Nagata, Yasuo Mori, Motohiro Nishida

研究成果: Contribution to journalArticle査読

1 被引用数 (Scopus)

抄録

Non-alcoholic steatohepatitis (NASH) is a disease that has progressed from non-alcoholic fatty liver disease (NAFLD) and is characterized by inflammation and fibrosis. Two transient receptor potential canonical (TRPC) subfamily members, TRPC3 and TRPC6 (TRPC3/6), reportedly participate in the development of fibrosis in cardiovascular and renal systems. We hypothesized that TRPC3/6 may also participate in NASH fibrosis. We evaluated the effects of TRPC3 or TRPC6 functional deficiency in a NASH mouse model using choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Wild-type (WT) and TRPC3 or TRPC6 gene-deficient (KO) mice were fed with CDAHFD or standard diet for 6 weeks. The CDAHFD-induced body weight loss in TRPC6 KO mice was significantly lower compared with WT mice with CDAHFD. CDAHFD treatment significantly increased TRPC3 mRNA expression level and tissue weight in WT liver, which were suppressed in TRPC3 KO mice. However, either systemic deletion of TRPC3 or TRPC6 failed to attenuate liver steatosis, inflammation and fibrosis. These results imply that TRPC3 and TRPC6 are unlikely to be involved in liver dysfunction and fibrosis of NASH model mice.

本文言語英語
ページ(範囲)431-436
ページ数6
ジャーナルBiological and Pharmaceutical Bulletin
44
3
DOI
出版ステータス出版済み - 3 1 2021

All Science Journal Classification (ASJC) codes

  • 薬理学
  • 薬科学

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