Pathological hypertrophy reverses β2-adrenergic receptor-induced angiogenesis in mouse heart

Physiological Reports
Qi XuXiao-Jun Du

Abstract

β-adrenergic activation and angiogenesis are pivotal for myocardial function but the link between both events remains unclear. The aim of this study was to explore the cardiac angiogenesis profile in a mouse model with cardiomyocyte-restricted overexpression of β2-adrenoceptors (β2-TG), and the effect of cardiac pressure overload. β2-TG mice had heightened cardiac angiogenesis, which was essential for maintenance of the hypercontractile phenotype seen in this model. Relative to controls, cardiomyocytes of β2-TGs showed upregulated expression of vascular endothelial growth factor (VEGF), heightened phosphorylation of cAMP-responsive-element-binding protein (CREB), and increased recruitment of phospho-CREB, CREB-binding protein (CBP), and p300 to the VEGF promoter. However, when hearts were subjected to pressure overload by transverse aortic constriction (TAC), angiogenic signaling in β2-TGs was inhibited within 1 week after TAC. β2-TG hearts, but not controls, exposed to pressure overload for 1-2 weeks showed significant increases from baseline in phosphorylation of Ca(2+)/calmodulin-dependent kinase II (CaMKIIδ) and protein expression of p53, reduction in CREB phosphorylation, and reduced abundance of phospho-CREB, p300 and CBP...Continue Reading

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Citations

Nov 4, 2004·Journal of Molecular and Cellular Cardiology·Xiao-Jun DuRobert M Graham
Oct 30, 2016·British Journal of Pharmacology·Sonia MaccariGiuseppe Marano
Feb 24, 2021·The Journal of Physiological Sciences : JPS·Shunsuke HyugaGeorge Gallos

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Methods Mentioned

BETA
transfection
immunoprecipitation
ChIP
PCR
transgenic

Software Mentioned

pro plus
GraphPad Prism
Image J
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Quantity One

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