Angiotensin II stimulates α-skeletal actin expression in cadiomyocytes in vitro and in vivo in the absence of hypertension

• Published in: Differentiation (London) Vol. 69; no. 1; pp. 66 - 74
• Main Authors: Clément, Sophie, Pellieux, Corinne, Chaponnier, Christine, Pedrazzini, Thierry, Gabbiani, Giulio
• Format: Journal Article
• Language: English
• Published: Berlin/Wien Elsevier B.V 01.12.2001; Blackwell Wissenschafts‐Verlag; Blackwell
• Subjects: Actins - metabolism; Angiotensin II - physiology; Animals; Base Sequence; Biological and medical sciences; cardiac hypertrophy; Cell Differentiation - physiology; Cell differentiation, maturation, development, hematopoiesis; Cell physiology; DNA Primers; Fundamental and applied biological sciences. Psychology; gene expression; Hypertension - metabolism; In Vitro Techniques; Mice; Mice, Transgenic; Molecular and cellular biology; Myocardium - cytology; Myocardium - metabolism; myocytes; Rats; Rats, Wistar; renin; Renin - genetics; TGF-β; TGF-β; cardiac hypertrophy; renin; gene expression; myocytes; Myoblast; In vivo
• ISSN: 0301-4681; 1432-0436
• DOI: 10.1046/j.1432-0436.2001.690107.x

Using a specific α-skeletal actin antibody, we have previously shown, that during hypertension-associated cardiac hypertrophy in the rat, the expression of α-skeletal actin in the myocardium is increased, but maintains focal distribution, compared to normotensive animals. In the present study, we have investigated whether α-skeletal actin expression can be induced in the absence of hypertension. For this purpose, we have examined transgenic mice overexpressing angiotensinogen exclusively in the heart. These animals are characterized by high cardiac angiotensin II levels and cardiac hypertrophy accompanied or not by high blood pressure depending on their genetic background, i.e. presence of one or two renin genes. α-Skeletal actin levels were highly increased in transgenic compared to wild-type myocardium independently of the number of renin genes, indicating that angiotensin II can stimulate α-skeletal actin expression in normotensive animals. Additional in vitro experiments using cultured mouse and rat cardiomyocytes showed that angiotension II not only increases α-skeletal actin expression but also induces an increase of its incorporation within II-bands compared to control cardiomyocytes. Angiotensin II increases also the expression of α-smooth muscle actin in sarcomeres of cardiomyocytes as well as in fibroblastic cells present within the culture.