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Angiotensin II Induces Translocation of Protein Kinase C α and ε in Neonatal Rat Cardiac Myocytes

Published online by Cambridge University Press:  02 July 2020

Tara A. Bullard
Affiliation:
Department of Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC, 29208
Edie Goldsmith
Affiliation:
Department of Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC, 29208
Robert L. Price
Affiliation:
Department of Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC, 29208
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Abstract

Angiotensin II (Ang II) plays an important role in heart development and has been shown to stimulate the formation of premyofibrils and differentiation of cardiac myocytes. Ang II signaling occurs through two types of receptors, the AT1 and AT2 receptors, both of which appear to play a role in the development of the myocardium. Through the use of specific Ang II receptor blockers it as been shown that blocking the AT1 receptor with Losartan (Merck) inhibits the formation of premyofibrils and sarcomere formation and that blocking the AT2 receptor with PD123,319 (Parke-Davis) inhibits the formation of trabeculae in the developing heart.

In a number of cases it has been shown that signal transduction mechanisms operate through different growth factor receptors and elicit specific responses within a cell type. Protein kinase C (PKC) is a family of closely related signal transduction enzymes that phosphorylate proteins on serine or threonine residues.

Type
Challenges of Confocal Microscopy in the 21st Century (Organized by S. Paddock)
Copyright
Copyright © Microscopy Society of America 2001

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References

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