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Quantitative trait loci associated with angiotensin II and high-salt diet induced acute decompensated heart failure in Balb/CJ mice
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.ORCID iD: 0000-0002-1110-9488
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.ORCID iD: 0000-0003-4675-1099
2019 (English)In: Physiological Genomics, ISSN 1094-8341, E-ISSN 1531-2267, Vol. 51, no 7, p. 279-289Article in journal (Refereed) Published
Abstract [en]

Genetic background of different mouse strains determines their susceptibility to disease. We have previously shown that Balb/CJ and C57BL/6J mice develop cardiac hypertrophy to the same degree when treated with a combination of angiotensin II and high-salt diet (ANG II+ Salt). but only Balb/CJ show impaired cardiac function associated with edema development and substantial mortality. We hypothesized that the different response to ANG II +Salt is due to the different genetic backgrounds of Balb/CJ and C57BL/6J. To address this we performed quantitative trait locus (QTL) mapping of second filial generation (F2) of mice derived from a backcross between Balb/CJ and first filial generation (Fl) of mice. Cardiac function was measured with echocardiography, glomerular filtration rate using FITC-inulin clearance, fluid and electrolyte balance in metabolic cages, and blood pressure with tail-cuff at baseline and on the fourth day of treatment with ANG II+Salt. A total of nine QTLs were found to be linked to different phenotypes in ANG II + Salt-treated F2 mice. A QTL on chromosome 3 was linked to cardiac output. and a QTL on chromosome 12 was linked to isovolumic relaxation time. QTLs on chromosome 2 and 3 were linked to urine excretion and sodium excretion. Eight genes located at the different QTLs contained coding nonsynonymous SNPs published in the mouse genome database that differ between Balb/CJ and C57BL/6J. In conclusion. ANG II+Salt-induced acute decompensation in Balb/CJ is genetically linked to several QTLs, indicating a multifaceted phenotype. The present study identified potential candidate genes that may represent important pathways in acute decompensated heart failure.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC , 2019. Vol. 51, no 7, p. 279-289
Keywords [en]
acute decompensated heart failure, angiotensin II, genetic susceptibility, high-salt diet, QTL
National Category
Physiology
Identifiers
URN: urn:nbn:se:uu:diva-391025DOI: 10.1152/physiolgenomics.00017.2019ISI: 000475942000003PubMedID: 31125294OAI: oai:DiVA.org:uu-391025DiVA, id: diva2:1344003
Funder
Åke Wiberg FoundationSwedish Heart Lung FoundationSwedish Society of MedicineSwedish Society for Medical Research (SSMF)Available from: 2019-08-20 Created: 2019-08-20 Last updated: 2019-08-20Bibliographically approved

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Becirovic Agic, MedihaJönsson, SofiaHultström, Michael

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