Both kappa and delta opioid receptors have been identified in the myocardial cell. These receptors ave coupled to phosphoinositide turnover and protein kinase C (PKC) activation and their stimulation affects the cytosolic Ca2+ and pH homeostasis as well as the contractility and the myofilament responsiveness to Ca2+. Both the proenkephalin and the prodynorphin gene are expressed in cardiac myocytes. These cells ave also able to synthetize and secrete dynorphin B, a biologically active end product of the prodynorphin gene binding selectively the kappa opioid receptor. Prodynorphin mRNA and dynorphin B expression are markedly increased in ventricular myocytes isolated from Syrian cardiomyopathic hamsters (the hypertrophic BIO 14.6 strain), as compared with normal cells. Nuclear PKC activation and intracellular Ca2+ overload have been shown to act as the two major signaling mechanisms involved in the increase in prodynorphin gene transcription observed in cardiomyopathic myocytes. In these cells, secreted dynorphin B activates kappa opioid receptors at the cell surface and elicits an autocrine loop, leading to an increase in nuclear PKC activity and to a tonic feed forward stimulation of prodynorphin gene transcription. The possibility that opioid genes may act in an autocrine fashion to affect myocardial Ca2+ homeostasis, growth, and differentiation is also discussed. (C) 1998, Elsevier Science Inc.

Opioid peptide gene expression in the myocardial cell / Ventura, C; Pintus, Gianfranco; Tadolini, B.. - In: TRENDS IN CARDIOVASCULAR MEDICINE. - ISSN 1050-1738. - 8:3(1998), pp. 102-110. [10.1016/S1050-1738(97)00140-0]

Opioid peptide gene expression in the myocardial cell

PINTUS, Gianfranco;
1998-01-01

Abstract

Both kappa and delta opioid receptors have been identified in the myocardial cell. These receptors ave coupled to phosphoinositide turnover and protein kinase C (PKC) activation and their stimulation affects the cytosolic Ca2+ and pH homeostasis as well as the contractility and the myofilament responsiveness to Ca2+. Both the proenkephalin and the prodynorphin gene are expressed in cardiac myocytes. These cells ave also able to synthetize and secrete dynorphin B, a biologically active end product of the prodynorphin gene binding selectively the kappa opioid receptor. Prodynorphin mRNA and dynorphin B expression are markedly increased in ventricular myocytes isolated from Syrian cardiomyopathic hamsters (the hypertrophic BIO 14.6 strain), as compared with normal cells. Nuclear PKC activation and intracellular Ca2+ overload have been shown to act as the two major signaling mechanisms involved in the increase in prodynorphin gene transcription observed in cardiomyopathic myocytes. In these cells, secreted dynorphin B activates kappa opioid receptors at the cell surface and elicits an autocrine loop, leading to an increase in nuclear PKC activity and to a tonic feed forward stimulation of prodynorphin gene transcription. The possibility that opioid genes may act in an autocrine fashion to affect myocardial Ca2+ homeostasis, growth, and differentiation is also discussed. (C) 1998, Elsevier Science Inc.
1998
Opioid peptide gene expression in the myocardial cell / Ventura, C; Pintus, Gianfranco; Tadolini, B.. - In: TRENDS IN CARDIOVASCULAR MEDICINE. - ISSN 1050-1738. - 8:3(1998), pp. 102-110. [10.1016/S1050-1738(97)00140-0]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11388/84527
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