Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 OC6.1

ECE2007 Oral Communications Cardiovascular endocrinology (7 abstracts)

Growth hormone-releasing hormone prevents cardiomyocyte apoptosis and activated PI3K/AKT, ERK1/2 and CREB signaling pathways

Riccarda Granata , Letizia Trovato , Silvia Destefanis , Fabio Settanni , Marta Annunziata , Davide Gallo & Ezio Ghigo


Dept. Internal Medicine, Div. Endcocrinology and Metabolism, University of Turin, Turin, Italy.

The hypothalamic hormone growth hormone-releasing hormone (GHRH), has been shown to function via its receptor splice variants as an autocrine/paracrine growth factor in normal and malignant cell lines and tissues, besides positively regulating growth hormone (GH) synthesis and secretion from the pituitary. Moreover, GHRH antagonists are known to suppress the proliferation of a wide variety of cancer cells through mechanisms yet to be fully elucidated. Aim of this study was to investigate the effect of GHRH on cell death and apoptosis induced by either serum deprivation or by the β adrenergic agonist isoproterenol (ISO) in rat H9c2 cardiomyocytes and in isolated adult rat cardiac myocytes. H9c2 cells and cardiac myocytes were cultured in serum-deprived medium for 48 h in the presence or absence of either ISO (100 μM) or GHRH (0.5 μM). RT-PCR analysis revealed the presence of GHRH receptor (GHRH-R) mRNA in both H9c2 cells and rat cardiac myocytes. GHRH (0.5 μM) significantly counteracted serum starvation- and ISO-induced cell death and apoptosis in both cell models. Further, either GHRH or isoproterenol induced ERK1/2 phosphorylation, whereas only GHRH activated Akt survival signaling pathway. Interestingly, both GHRH and ISO induced cAMP increase and phosphorylation of its down-stream transcription factor cyclic AMP response element-binding protein (CREB) in H9c2 cells. Finally, the GHRH-R antagonist JV-1-36 completely abolished the survival effects of GHRH in H9c2 cells, under both serum starvation- and ISO-induced cell death and apoptosis.

These results indicate that GHRH is a survival factor for cardiac myocytes. Moreover, they suggest that this molecule may play a role in the prevention of cardiac cell loss in pathological conditions that ultimately lead to the development of heart failure.

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