ArticleAmerican journal of hypertension2017
Differential Expression of Hypertensive Phenotypes in BXD Mouse Strains in Response to Angiotensin II.
Article in American journal of hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Essential resources and best practices for laboratory mouse research.Molecules and cells · 2025Review
- Combination of Perindopril Erbumine and Huangqi-Danshen Decoction Protects Against Chronic Kidney Disease via Sirtuin3/Mitochondrial Dynamics Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Genetically modified mouse models to help fight COVID-19.Nature protocols · 2020Review
- The Genetic Dissection ofFrontiers in cardiovascular medicine · 2020Article
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Abstract
backgroundBesides environmental risk factors, genetic factors play a crucial role in the pathogenesis of primary hypertension. The current study is to unravel whether hypertensive phenotypes vary in mice with different genetic background.
methodsHypertension was induced in C57BL/6J (B6), DBA/2J (D2), and 25 BXD strains by administrating angiotensin (Ang)II (2.5 mg/kg/day infused by osmotic minipump) for 4 weeks. Systolic blood pressure was monitored before (baseline) and after 4 weeks of AngII treatment by tail cuff. Cardiac and renal fibrosis was evaluated by picrosirius red staining and collagen volume fraction (CVF) was quantitated using imaging analyzing system; cardiac transforming growth factor (TGF)-β gene expression was monitored by RT-PCR, and inflammatory response was detected by immunohistochemical ED-1 staining.
resultsAngII infusion caused hypertension in all strains. However, blood pressure elevation was more evident in the D2 strain than the B6 group, while it was widely variable among BXD strains. Furthermore, chronic AngII treatment lead to development of hypertensive cardiac and renal diseases. Cardiac and renal CVF levels in the D2 strain was significantly higher than the B6 cohort, whereas these varied vastly across BXD strains. Moreover, cardiac TGF-β mRNA levels were markedly diverse among various mouse strains.
conclusionOur study unequivocally demonstrates that in response to AngII, BXDs with different genetic background expressed hypertension phenotypes with varied degree in severity. It implicates that genomics contribute to pathogenesis of primary hypertension. Building upon the genotype and hypertensive phenotypes, the BXD cohort can be further exploited experimentally to identify genes that influence blood pressure.
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