Angiotensin II stimulates α-skeletal actin expression in cadiomyocytes in vitro and in vivo in the absence of hypertension
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 ha...
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Published in | Differentiation (London) Vol. 69; no. 1; pp. 66 - 74 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Wien
Elsevier B.V
01.12.2001
Blackwell Wissenschafts‐Verlag Blackwell |
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Abstract | 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. |
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AbstractList | 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. Using a specific alpha-skeletal actin antibody, we have previously shown, that during hypertension-associated cardiac hypertrophy in the rat, the expression of alpha-skeletal actin in the myocardium is increased, but maintains focal distribution, compared to normotensive animals. In the present study, we have investigated whether alpha-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. Alpha-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 alpha-skeletal actin expression in normotensive animals. Additional in vitro experiments using cultured mouse and rat cardiomyocytes showed that angiotension II not only increases alpha-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 alpha-smooth muscle actin in sarcomeres of cardiomyocytes as well as in fibroblastic cells present within the culture. 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. |
Author | Pedrazzini, Thierry Clément, Sophie Pellieux, Corinne Chaponnier, Christine Gabbiani, Giulio |
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Keywords | TGF-β cardiac hypertrophy renin gene expression myocytes Myoblast In vivo |
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Snippet | Using a specific α-skeletal actin antibody, we have previously shown, that during hypertension-associated cardiac hypertrophy in the rat, the expression of... Using a specific α‐skeletal actin antibody, we have previously shown, that during hypertension‐associated cardiac hypertrophy in the rat, the expression of... Using a specific alpha-skeletal actin antibody, we have previously shown, that during hypertension-associated cardiac hypertrophy in the rat, the expression of... |
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SubjectTerms | 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 |
Title | Angiotensin II stimulates α-skeletal actin expression in cadiomyocytes in vitro and in vivo in the absence of hypertension |
URI | https://dx.doi.org/10.1046/j.1432-0436.2001.690107.x https://onlinelibrary.wiley.com/doi/abs/10.1046%2Fj.1432-0436.2001.690107.x https://www.ncbi.nlm.nih.gov/pubmed/11776396 https://search.proquest.com/docview/72378779 |
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