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Impaired left-ventricular cardiac function in male GPR30-deficient mice.

Martina Delbeck, Stefan Golz, Richardus Vonk, Wiebke Janssen, Tim Hucho, Jörg Isensee, Stefan Schäfer, Christiane Otto

Cardiology Research, Bayer Schering Pharma AG, 42096 Wuppertal, Germany.

Journal Article: Molecular Medicine Reports 01/2011; 4(1):37-40. DOI: 10.3892/mmr.2010.402

Abstract

G-protein-coupled receptor 30 (GPR30) has been reported to act as a membrane-bound estrogen receptor that is involved in the mediation of non-genomic estradiol signalling. In this study, we demonstrated that male, but not female, GPR30-deficient mice suffer from impaired left‑ventricular cardiac function. Left ventricles from male mutant mice were enlarged. There were no malformations in the valves or outflow tract of the heart. Both the contractility and relaxation capacity of the left ventricle were reduced, leading to increased left‑ventricular end-diastolic pressure in GPR30-deficient mice. In conclusion, our data support a role for GPR30 in the gender-specific aspects of heart failure.

Source: PubMed

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Keywords

contractility
 
GPR30-deficient mice
 
heart failure
 
left‑ventricular cardiac function
 
left‑ventricular end-diastolic pressure
 
mediation
 
outflow tract
 
relaxation capacity
 
valves