The possible involvement of tensin2 in the expression and extension of nephrin by glomerular podocytes in mice

• Kato Takashi

  Division of Molecular Regenerative Medicine, Department of Biochemistry and Molecular Biology, Osaka University Graduate School of Medicine The Institute of Experimental Animal Sciences, Osaka University Graduate School of Medicine Department of Pharmacology, Graduate School of Medicine, Kyoto University

• Mizuno Shinya

  Division of Molecular Regenerative Medicine, Department of Biochemistry and Molecular Biology, Osaka University Graduate School of Medicine

• Taketo Makoto Mark

  Department of Pharmacology, Graduate School of Medicine, Kyoto University

• Kurosawa Tsutomu Miki

  The Institute of Experimental Animal Sciences, Osaka University Graduate School of Medicine

抄録

The prevalence of chronic kidney disease (CKD) is increasing worldwide and proteinuria is a critical prognostic indicator of CKD. Nephrin is produced by podocytes and functions as a slit barrier for inhibition of proteinuria. Nephrin expression is frequently decreased in CKD patients. Nevertheless, the mechanism by which nephrin declines during CKD-related pathological states remains to be determined. Using tensin2-deficient mice (ICGN/Oa strain), we provide evidence that tensin2 is important for glomerular nephrin expression in vivo. In heterozygous mice with a single mutated tensin2 allele, nephrin expression was maintained, while albuminuria was not observed. In contrast, nephrin expression was impaired, especially in the central zones of glomeruli of homozygous mice (with double mutated tensin2 alleles), even at one week after birth. In homozygous mice, extension of synaptopodin, a key actin-associated protein, was also suppressed in the central zone of glomerular tufts. Consistent with the loss of nephrin and synaptopodin expression, severe albuminuria was detected in homozygous ICGN/Oa mice. Therefore, we suggested that tensin2 is involved in expression and extension of nephrin, while tensin2 deficiency may result in proteinuria, associated with the loss of slit integrity.

収録刊行物

• Biomedical Research

  Biomedical Research 29 (6), 279-287, 2008

  バイオメディカルリサーチプレス

キーワード

• General Biochemistry, Genetics and Molecular Biology
• General Medicine

詳細情報

• CRID: 1390001204902448768
• NII論文ID: 130004470727
• DOI: 10.2220/biomedres.29.279
• ISSN: 1880313X
• ISSN: 03886107
• Web Site: https://search.jamas.or.jp/link/ui/2009159018
• 本文言語コード: en
• データソース種別:
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