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10.1186/s12863-016-0378-1

http://scihub22266oqcxt.onion/10.1186/s12863-016-0378-1
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suck abstract from ncbi


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pmid27230548
      BMC+Genet 2016 ; 17 (1 ): 69
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  • Mouse chromosome 2 harbors genetic determinants of resistance to podocyte injury and renal tubulointerstitial fibrosis #MMPMID27230548
  • Sasaki H ; Kimura J ; Nagasaki K ; Marusugi K ; Agui T ; Sasaki N
  • BMC Genet 2016[May]; 17 (1 ): 69 PMID27230548 show ga
  • BACKGROUND: Tensin2 deficiency results in alterations in podocytes and subsequent glomerular and tubulointerstitial injuries. However, this pathology is critically dependent on genetic background. While the Tensin2-deficient podocytes of resistant murine strains, including C57BL/6J mice, remain almost intact, susceptible murine strains with Tensin2 deficency, including ICGN mice, develop chronic kidney disease following alterations in the podocyte foot processes. In a previous study, genome-wide linkage analysis was utilized to identify the quantitative trait loci associated with the disease phenotypes on mouse chromosome 2. This study investigated the disease phenotypes of chromosome 2 consomic and subcongenic strains. RESULTS: ICGN consomic mice introgressed with chromosome 2 from the C57BL/6J mouse were generated and found to exhibit milder renal failure than that in ICGN mice. We developed 6 subcongenic strains that carry C57BL/6J-derived chromosomal segments from the consomic strain. One showed significantly milder albuminuria, another showed significantly milder tubulointerstitial injury, and the both showed significantly milder glomerular injury. CONCLUSIONS: These data indicate that mouse chromosome 2 harbors two major genes associated with the severities of nephropathy induced by Tensin2 deficiency. The proximal region on chromosome 2 contributes to the resistance to tubulointerstitial fibrosis. In contrast, the distal region on chromosome 2 contributes to the resistance to podocyte injury. This study would be helpful to discover the biological mechanism underlying the renal injury, and may lead to the identification of therapeutic targets.
  • |Animals [MESH]
  • |Chromosome Mapping [MESH]
  • |Chromosomes, Mammalian/*genetics [MESH]
  • |Disease Resistance/*genetics [MESH]
  • |Female [MESH]
  • |Fibrosis [MESH]
  • |Genetic Loci/genetics [MESH]
  • |Homozygote [MESH]
  • |Kidney Tubules/*pathology [MESH]
  • |Mice [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Podocytes/*pathology [MESH]


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