論文

査読有り
2015年

Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the mouse

BIOMEDICAL RESEARCH-TOKYO
  • Hayato Sasaki
  • ,
  • Kiyoma Marusugi
  • ,
  • Junpei Kimura
  • ,
  • Hiroshi Kitamura
  • ,
  • Ken-Ichi Nagasaki
  • ,
  • Daisuke Torigoe
  • ,
  • Takashi Agui
  • ,
  • Nobuya Sasaki

36
5
開始ページ
323
終了ページ
330
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.2220/biomedres.36.323
出版者・発行元
BIOMEDICAL RESEARCH PRESS LTD

Tensin2 (Tns2) is thought to be a component of the cytoskeletal structures linking actin filaments with focal adhesions and is known to play a role as an intracellular signal transduction mediator through integrin in podocytes, although the mechanism by which it functions remains unclear. A Tns2-null mutation (nph) leads to massive albuminuria following podocyte foot process effacement in the ICGN mice, the origin of the mutation, and the DBA/2J (D2) mice, but not in the C57BL/6J (B6) mice or 129(+Ter)/SvJcl (129T) mice. Elucidating the reasons for these differences in diverse genetic backgrounds could help in unraveling Tns2 function in podocytes. We produced congenic mice in which Tns2(nph) was introgressed into a FVB/NJ background (FVB-Tns2(nph)), and evaluated the progression of kidney disease. FVB-Tns2(nph) mice developed albuminuria, renal fibrosis and renal anemia as seen in ICGN mice. The FVB-Tns2(nph) mice demonstrated podocyte foot process alteration under an electron microscope by as early as 4 weeks of age. This revealed that FVB strain is susceptible to Tns2-deficiency.

Web of Science ® 被引用回数 : 9

リンク情報
DOI
https://doi.org/10.2220/biomedres.36.323
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26522149
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000366568100004&DestApp=WOS_CPL
ID情報
  • DOI : 10.2220/biomedres.36.323
  • ISSN : 0388-6107
  • eISSN : 1880-313X
  • PubMed ID : 26522149
  • Web of Science ID : WOS:000366568100004

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