Mapping quantitative trait loci for proteinuria-induced renal collagen deposition | Zendy

Nobutaka Kato | Zendy; Yusuke Watanabe | Zendy; Yoichi Ohno | Zendy; Tsutomu Inoue | Zendy; Yoshihiko Kanno | Zendy; Hiromichi Suzuki | Zendy; Hirokazu Okada | Zendy

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Mapping quantitative trait loci for proteinuria-induced renal collagen deposition

Author(s) -

Nobutaka Kato,

Yusuke Watanabe,

Yoichi Ohno,

Tsutomu Inoue,

Yoshihiko Kanno,

Hiromichi Suzuki,

Hirokazu Okada

Publication year - 2008

Publication title -

kidney international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.499

H-Index - 276

eISSN - 1523-1755

pISSN - 0085-2538

DOI - 10.1038/ki.2008.7

Subject(s) - quantitative trait locus , proteinuria , biology , fibrosis , kidney disease , kidney , genetic linkage , pathology , medicine , endocrinology , genetics , gene

The progression of chronic kidney disease is a complex process influenced by genetic factors. Proteinuria is a predictor of functional deterioration and an accelerator of disease progression through renal parenchymal damage and interstitial fibrosis. To determine genetic components that might mediate renal fibrosis due to proteinuria, we mapped loci influencing the phenotype of two mouse strains differing in proteinuria-induced renal type I collagen (COLI) deposition. Collagen I deposition in 129S1/svImJ and C57BL/6J mice differs significantly among tested strains. We backcrossed 120 hemi-nephrectomized (129S1/svImJ x C57BL/6J) F1 x 129S1/svImJ backcrossed mice loaded with bovine serum albumin giving rise to proteinuria and renal COLI deposition. Quantitative trait loci (QTL) mapping was performed and our analysis identified one suggestive linkage for renal COLI deposition peaking at 87 cM near D2Mit224 (logarithm of odds: 2.41) on Chr 2. In silico analysis uncovered nine candidate genes. Hence, although more studies are needed, these QTL provide an initial cue to subsequent gene discovery, which might help unravel the genetics of renal fibrosis.

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