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

Delbeck, M.; Golz, S.; Vonk, R.; Janssen, W.; Hucho, T.; Isensee, J.; Schafer, S.; Otto, C.

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

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Isensee, J.
Signal Transduction in Mental Retardation and Pain (Tim Hucho), Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Delbeck, M., Golz, S., Vonk, R., Janssen, W., Hucho, T., Isensee, J., et al. (2011). Impaired left-ventricular cardiac function in male GPR30-deficient mice. Mol Med Report, 4(1), 37-40. Retrieved from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21461560.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7969-D

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 leftventricular 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 leftventricular end-diastolic pressure in GPR30-deficient mice. In conclusion, our data support a role for GPR30 in the gender-specific aspects of heart failure.