Hormone therapy in men—increased risk of cardiac allograft rejection?

Tandler, R.; Kondruweit, M.; Fischlein, T; Weyand, Michael

doi:10.1016/s1053-2498(02)00639-3

Cited by 5 publications

(8 citation statements)

References 3 publications

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“…The present study suggests that that GnRH has positive cardiomyocyte contractile effects in the mouse. This effect appears specific to the intact GnRH molecule because the enzymatically cleaved GnRH product, GnRH- [1][2][3][4][5], a pentapeptide with biological activity independent of the GnRH receptor (30), failed to affect cardiomyocyte mechanical responses, whereas the GnRH type I receptor antagonist, cetrorelix, blocked the GnRH-mediated mechanical response. These observations favour a GnRH receptor-mediated mechanism for the GnRH-modulated cardiac contractile response.…”

Section: Discussionmentioning

confidence: 99%

“…The GnRHinduced cardiomyocyte mechanical responses were abolished or significantly attenuated by cetrorelix and H89 but not chelerythrine, suggesting an involvement of GnRH receptor and PKA (but unlikely PKC) in the GnRH-elicited cardiomyocyte contractile responses. GnRH- [1][2][3][4][5] had no effect on cardiomyocytes (Fig. 3).…”

Section: Effect Of Cetrorelix Protein Kinase Inhibitors Andmentioning

confidence: 92%

“…GnRH- [1][2][3][4][5] In the absence of GnRH, cetrorelix, H89 and chelerythrine chloride had no overt effect on cell shortening over 30 min (Fig. 3).…”

Section: Effect Of Cetrorelix Protein Kinase Inhibitors Andmentioning

confidence: 93%

“…These pharmacological agents were all applied for 20 min alone and then in the presence or absence of GnRH (1 pg ⁄ ml) for 10 min before the 0.5-Hz stimulation. GnRH can be enzymatically cleaved into GnRH- [1][2][3][4][5], which is a pentapeptide with biological activity independent of the GnRH receptor (30). To investigate whether the observed effects could be mediated by this pentapeptide, GnRH- [1][2][3][4][5] was synthesised (Michael Flora, Biomedical Instrumentation Center, Uniformed Services University of the Health Sciences, Bethesda, MD, USA) and applied (300 pg ⁄ ml) to cardiomyocytes for 10 min before the 0.5-Hz stimulation.…”

Section: Effect Of Cetrorelix Protein Kinase Inhibitors and Gnrh-[1-5]mentioning

confidence: 99%

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The Heart: A Novel Gonadotrophin-Releasing Hormone Target

Dong

Skinner

et al. 2011

Journal of Neuroendocrinology

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Gonadotrophin-releasing hormone (GnRH) is a hypothalamic hormone transported by the hypophyseal portal bloodstream to the pituitary gland, where it binds to GnRH receptors. However, GnRH receptors are expressed in multiple extrapituitary tissues, although their physiological relevance is not fully understood. GnRH agonists are employed extensively in steroid deprivation therapy, especially to suppress testosterone in prostate cancer. Because GnRH agonist treatment is associated with increased coronary heart disease and myocardial infarction, we investigated the impact of GnRH on cardiomyocyte contractile function. Cardiomyocytes were isolated from mouse hearts and mechanical and intracellular Ca(2+) properties were evaluated, including peak shortening amplitude (PS), time-to-PS (TPS), time-to-90% relengthening (TR(90) ), maximal velocity of shortening/relengthening (± dLdt), electrically-stimulated rise in Fura-2 fluorescence intensity (ΔFFI) and Ca(2+) decay. GnRH (1 ng/ml) increased PS, ± dL/dt, resting FFI and ΔFFI, and prolonged TPS, TR(90) and Ca(2+) decay time, whereas 1 pg/ml GnRH affected all these cardiomyocyte variables, except TPS, resting FFI and ΔFFI. A concentration of 1 fg/ml GnRH and the GnRH cleavage product, GnRH-[1-5] (300 pg/ml), had no effect on any cardiomyocyte parameter. The 1 pg/ml GnRH-elicited responses were attenuated by the GnRH receptor antagonist cetrorelix (10 μm), the protein kinase A (PKA) inhibitor H89 (1 μm) but not the protein kinase C inhibitor chelerythrine chloride (1 μm). These data revealed that GnRH is capable of regulating cardiac contractile function via a GnRH receptor/PKA-dependent mechanism. If present in the human heart, dysfunction of such a system may play an important role in cardiac pathology observed in men treated with GnRH agonists for prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Effect Of Cetrorelix Protein Kinase Inhibitors Andmentioning

confidence: 92%

“…GnRH- [1][2][3][4][5] In the absence of GnRH, cetrorelix, H89 and chelerythrine chloride had no overt effect on cell shortening over 30 min (Fig. 3).…”

Section: Effect Of Cetrorelix Protein Kinase Inhibitors Andmentioning

confidence: 93%

Section: Effect Of Cetrorelix Protein Kinase Inhibitors and Gnrh-[1-5]mentioning

confidence: 99%

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The Heart: A Novel Gonadotrophin-Releasing Hormone Target

Dong

Skinner

et al. 2011

Journal of Neuroendocrinology

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“…Schofield et al reported 3 cases of acute cardiac rejection that were temporally related to the administration of leuprolide acetate or testosterone in adult men, underscoring the importance of assessing the immune effects of non-cardiac drugs. 15,16 The effect of GH on graft vasculopathy is not known. In a small patient series, Meiser and colleagues reported no difference in 1-and 4-year survival in patients receiving angiopeptin, a stable analog of somatostatin (a GH inhibitor with anti-proliferative effects), compared with placebo.…”

Section: Discussionmentioning

confidence: 99%

Effects of Growth Hormone Therapy in Children After Cardiac Transplantation

Mital

Andron

Lamour

et al. 2006

The Journal of Heart and Lung Transplantation

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Expression and tissue localization of renalase, a novel soluble FAD-dependent protein, in reproductive/steroidogenic systems

et al. 2012

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Renalase was initially identified in human kidney as a soluble monoamine oxidase. Here we show that renalase is predominantly expressed in reproductive/steroidogenic systems, with particularly substantial expression in oocytes, granulosa, interstitial and luteal cells of ovary, spermatogenic cells of testis, and cortex of adrenal gland, suggesting its function(s) in maturation of germ cells and steroid hormone regulation. Renalase expression increases in testes and ovaries as mice develop and its expression is further enhanced in the ovaries of pregnant mice, indicating an activity of renalase in reproduction. Gonadotropin-releasing hormone (GnRH) antagonist, cetrorelix, repressed renalase expression in mice ovaries and testes, suggesting that steroids regulate renalase expression. Leptin is an effector and modulator of steroid hormones and reproduction. Surprisingly, knockout of leptin causes a dramatic increase of renalase expression in mice testes. Taken together, our results suggest that reproductive/steroidogenic systems are also the sources for renalase secretion and renalase may play a critical role in reproduction and hormone regulation. This provides a novel insight into understanding the function of renalase.

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Hormone therapy in men—increased risk of cardiac allograft rejection?

Cited by 5 publications

References 3 publications

The Heart: A Novel Gonadotrophin-Releasing Hormone Target

The Heart: A Novel Gonadotrophin-Releasing Hormone Target

Effects of Growth Hormone Therapy in Children After Cardiac Transplantation

Expression and tissue localization of renalase, a novel soluble FAD-dependent protein, in reproductive/steroidogenic systems

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