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Quantitative Trait Loci for Resistance to the Congenital Nephropathy in Tensin 2-Deficient Mice

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Title: Quantitative Trait Loci for Resistance to the Congenital Nephropathy in Tensin 2-Deficient Mice
Authors: Sasaki, Hayato Browse this author
Sasaki, Nobuya Browse this author →KAKEN DB
Nishino, Tomohiro Browse this author
Nagasaki, Ken-ichi Browse this author
Kitamura, Hiroshi Browse this author →KAKEN DB
Torigoe, Daisuke Browse this author
Agui, Takashi Browse this author →KAKEN DB
Issue Date: 26-Jun-2014
Publisher: Public Library of Science
Journal Title: PLOS ONE
Volume: 9
Issue: 6
Start Page: e99602
Publisher DOI: 10.1371/journal.pone.0099602
Abstract: The ICR-derived glomerulonephritis (ICGN) mouse is a chronic kidney disease (CKD) model that is characterized histologically by glomerulosclerosis, vascular sclerosis and tubulointerstitial fibrosis, and clinically by proteinuria and anemia, which are common symptoms and pathological changes associated with a variety of kidney diseases. Previously, we performed a quantitative trait locus (QTL) analysis to identify the causative genes for proteinuria in ICGN mice, and found a deletion mutation of the tensin 2 gene (Tns2(nph), MGI no: 2447990). Interestingly, the congenic strain carrying the Tns2(nph) mutation on a C57BL/6J (B6) genetic background exhibited milder phenotypes than did ICGN mice, indicating the presence of several modifier genes controlling the disease phenotype. In this study, to identify the modifier/resistant loci for CKD progression in Tns2-deficient mice, we performed QTL analysis using backcross progenies from susceptible ICGN and resistant B6 mice. We identified a significant locus on chromosome (Chr) 2 (LOD = 5.36; 31 cM) and two suggestive loci on Chrs 10 (LOD = 2.27; 64 cM) and X (LOD = 2.65; 67 cM) with linkage to the severity of tubulointerstitial injury. One significant locus on Chr 13 (LOD = 3.49; approximately 14 cM) and one suggestive locus on Chr 2 (LOD = 2.41; 51 cM) were identified as QTLs for the severity of glomerulosclerosis. Suggestive locus in BUN was also detected in the same Chr 2 region (LOD = 2.34; 51 cM). A locus on Chr 2 (36 cM) was significantly linked with HGB (LOD = 4.47) and HCT (LOD = 3.58). Four novel epistatic loci controlling either HGB or tubulointerstitial injury were discovered. Further genetic analysis should lead to identification of CKD modifier gene(s), aiding early diagnosis and providing novel approaches to the discovery of drugs for the treatment and possible prevention of kidney disease.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/56860
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 安居院 高志

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