<b>Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the </b><b>mouse </b>

• SASAKI Hayato

  Laboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University Laboratory of Laboratory Animal Science and Medicine, Graduate School of Veterinary Medicine, Hokkaido University

• MARUSUGI Kiyoma

  Laboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University

• KIMURA Junpei

  Laboratory of Anatomy, Graduate School of Veterinary Medicine, Hokkaido University

• KITAMURA Hiroshi

  Department of Veterinary Physiology, School of Veterinary Medicine, Rakuno Gakuen University

• NAGASAKI Ken-Ichi

  Section of Biological Safety Research, Chitose Laboratory, Japan Food Research Laboratories

• TORIGOE Daisuke

  Laboratory of Laboratory Animal Science and Medicine, Graduate School of Veterinary Medicine, Hokkaido University

• AGUI Takashi

  Laboratory of Laboratory Animal Science and Medicine, Graduate School of Veterinary Medicine, Hokkaido University

• SASAKI Nobuya

  Laboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University

Bibliographic Information

Other Title

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

Abstract

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.

Journal

• Biomedical Research

  Biomedical Research 36 (5), 323-330, 2015

  Biomedical Research Press

Keywords

• General Biochemistry, Genetics and Molecular Biology
• General Medicine

Details

• CRID: 1390001204900578560
• NII Article ID: 130005106627
• DOI: 10.2220/biomedres.36.323
• ISSN: 1880313X
• ISSN: 03886107
• HANDLE: 10659/4992
• PubMed: 26522149
• Web Site: https://rakuno.repo.nii.ac.jp/records/2226
• Web Site: https://www.jstage.jst.go.jp/article/biomedres/36/5/36_323/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2016055276
• Text Lang: en
• Data Source:
  • JaLC
  • IRDB
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed