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