AutoCAD Crack With License Code
AutoCAD Crack With License Code
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Cardiac myocyte-specific overexpression of transforming growth factor-beta type II receptor in a genetic model of pressure overload cardiac hypertrophy. We investigated the role of transforming growth factor-beta (TGF-beta) type II receptor (TbetaR-II) in cardiac myocytes, using a gene transfer approach in a genetic model of cardiac hypertrophy and dysfunction. Transgenic mice were generated by microinjection of an expression construct containing the cardiomyocyte-specific beta-myosin heavy chain promoter and an internal ribosome entry site upstream of a cDNA encoding the murine TbetaR-II cDNA. These animals were viable and fertile, and a Western blot analysis revealed a dose-dependent increase in TbetaR-II protein expression. Immunohistochemical staining revealed a TbetaR-II-specific increase in myocyte size and surface area. The increase in myocyte size was associated with increased cardiac hypertrophy in animals maintained under normal pressure, whereas the response to pressure overload was blunted in TbetaR-II-overexpressing animals. Chronic volume overload resulted in cardiac dysfunction and increased fibrosis in both wild-type and transgenic animals. However, whereas systolic function was restored in wild-type animals, cardiac dysfunction persisted in the TbetaR-II-overexpressing animals. The persistence of cardiac dysfunction in the TbetaR-II-overexpressing animals was associated with fibrosis and inflammatory changes in the myocardium. These results demonstrate that TbetaR-II is essential for the development of cardiac hypertrophy and failure in this genetic model of cardiac hypertrophy and suggest that this receptor may be important in the myocyte response to other forms of cardiac injury.
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