Biomedical Research
Online ISSN : 1880-313X
Print ISSN : 0388-6107
ISSN-L : 0388-6107
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Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the mouse
Hayato SASAKIKiyoma MARUSUGIJunpei KIMURAHiroshi KITAMURAKen-Ichi NAGASAKIDaisuke TORIGOETakashi AGUINobuya SASAKI
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2015 年 36 巻 5 号 p. 323-330

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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 Tns2nph was introgressed into a FVB/NJ background (FVB-Tns2nph), and evaluated the progression of kidney disease. FVB-Tns2nph mice developed albuminuria, renal fibrosis and renal anemia as seen in ICGN mice. The FVB-Tns2nph 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.

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© 2015 Biomedical Research Press
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