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Evaluation of Pathological Association between Stroke-Related QTL and Salt-Induced Renal Injury in Stroke-Prone Spontaneously Hypertensive Rat.
Reza, Mohammad Farhadur; Ngarashi, Davis; Koike, Masamichi; Misumi, Masaki; Ohara, Hiroki; Nabika, Toru.
Afiliación
  • Reza MF; Department of Functional Pathology, Shimane University Faculty of Medicine, Izumo, Japan.
  • Ngarashi D; Department of Functional Pathology, Shimane University Faculty of Medicine, Izumo, Japan.
  • Koike M; Department of Oncology, Shimane University Faculty of Medicine, Izumo, Japan.
  • Misumi M; Department of Oncology, Shimane University Faculty of Medicine, Izumo, Japan.
  • Ohara H; Department of Functional Pathology, Shimane University Faculty of Medicine, Izumo, Japan.
  • Nabika T; Department of Functional Pathology, Shimane University Faculty of Medicine, Izumo, Japan.
Biomed Res Int ; 2019: 5049746, 2019.
Article en En | MEDLINE | ID: mdl-30792992
The stroke-prone spontaneously hypertensive rat (SHRSP) suffers from severe hypertension and hypertensive organ damage such as cerebral stroke and kidney injury under salt-loading. By a quantitative trait locus (QTL) analysis between SHRSP and SHR (the stroke-resistant parental strain of SHRSP), two major QTLs for stroke susceptibility were identified on chromosomes 1 and 18 of SHRSP, which were confirmed in congenic strains constructed between SHRSP and SHR. As the progression of renal dysfunction was suggested to be one of the key factors inducing stroke in SHRSP, we examined effects of the stroke-related QTLs on kidney injury using two congenic strains harboring either of SHRSP-derived fragments of chromosomes 1 and 18 in the SHR genome. The congenic strains were challenged with 1% NaCl solution for 4 weeks; measurement of systolic blood pressure and urinary isoprostane level (a marker for oxidative stress) and evaluation of renal injury by quantification of genetic marker expression and histological examination were performed. We found that the congenic rats with SHRSP-derived fragment of chromosome 18 showed more severe renal damage with higher expression of Col1α-1 (a genetic marker for renal fibrosis) and higher urinary isoprostane level. In contrast, the fragment of chromosome 1 from SHRSP did not give such effects on SHR. Blood pressure was not greater in either of the congenic strains when compared with SHR. We concluded that the QTL region on chromosome 18 might deteriorate salt-induced renal injury in SHR through a blood pressure-independent mechanism.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular / Sitios de Carácter Cuantitativo / Lesión Renal Aguda / Hipertensión Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals / Humans Idioma: En Revista: Biomed Res Int Año: 2019 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Accidente Cerebrovascular / Sitios de Carácter Cuantitativo / Lesión Renal Aguda / Hipertensión Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals / Humans Idioma: En Revista: Biomed Res Int Año: 2019 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos