Proteinuria-induced chronic kidney disease in the ICGN/Oa mice with a mutation of Tensin2 gene.

摘要: ICGN/Oa mice are used to study the pathophysiological mechanisms underlying proteinuria-induced chronic kidney disease (CKD). Recently, a mutation of tensin2 gene (Tns2) was suggested be responsible for proteinuria in inbred ICGN mice. We identified wild-type (+/+), heterozygous (+/nep), and homozygous (nep/nep) by PCR assay. The homozygotes developed proteinuria, resulting nephrotic syndrome (NS) as early 5 weeks CKD 15 weeks. However, heterozygotes did not show symptoms these renal failures. These results indicate that is necessary develop CKD. Furthermore, we examined time course tubulointerstitial fibrosis kinetics tubular epithelial cells (TECs) using immunohistochemical TUNEL assays. In parenchyma five-week-old homozygotes, expression α-SMA type I collagen were higher than those age-matched wild-type. ...