By B. Swynghedauw MD, PhD (auth.), Prof. Dr. med. J. Holtz, PD Dr. H. Drexler, Prof. Dr. H. Just (eds.)
Traditionally, cardiac hypertrophy is considered an version of the center to everlasting mechanical overload. whatever the incontrovertible fact that many various and infrequently unknown fundamental reasons can lead to center failure, mechanical overload and myocardial hypertrophy is located in just about all sorts of appear persistent middle failure (apart from failure because of extramyocardial stumbling blocks to influx or to relaxation). despite the fact that, the reactive growth of myocardial mass in accordance with an greater hemodynamic burden seems to be a double-edged sword. evidently, the hypertrophy is helping to lessen the improved ventricular wall tension in middle failure by means of including contractile devices to the overdistended chamber wall. despite the fact that, in recent times it grew to become transparent that this adaptive hypertrophic procedure is very advanced and will comprise challenging points. The adaptive hypertrophy comprises proliferation of the nonmyocyte cardiac cells in addition to enormous changes within the phenotype of the growing to be myocytes because of differential adjustments in gene expression.
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Extra info for Cardiac Adaptation in Heart Failure: Risks due to myocardial phenotype changes
The sham operation value, shown at the left for each panel, denotes the mean ± SE of 34 samples, which did not vary with time. 05. (B, D, F) Correlation of a-actin gene induction with the extent of ventricular hypertrophy. Individual values are shown for each animal subjected to (0) sham operation (N = 34) or (e) aortic constriction (N = 31). Correlation coefficients were derived from animals subjected to coarctation for 2 or more days. D. Schneider et al. and negative control differs both from the global suppression of muscle-specific genes by these growth factors in skeletal muscle myoblasts and from the refractoriness of terminally differentiated skeletal muscle myotubes to regulation by these peptides (8, 37).
A) Cardiac myocytes were transfected with the - 202/ - 11 or - 2000/ - 11 promoter. CAT activity was normalized to expression of each promoter, respectively, in vehicle-treated cells. Black) recombinant aFGF, 25 ng ' ml- I; grey) recombinant bFGF, 25ng·ml - l . B) Regulation of skeletal and cardiac IX-actin steady state mRNA abundance in cardiac muscle by aFGF, bFGF, TGFfJl , and recombinant FGFs (abscissa) is highly correlated with control of exogenous promoters (ordinate). D. Schneider et al.
As shown in Fig. 2, the activated mutant of the f3-PKC isoform increased expression from the f3-MHC promoter, and was more than twice as potent as activated a-PKC. These data provide the first direct evidence that the f3-PKC isozyme is in a pathway regulating transcription of the f3-MHC isogene and are the first to suggest functional differences among PKC isoforms in cardiac myocytes. The specific DNA sequences in the f3-MHC promoter that mediate the f3-PKC response are presently under study in our laboratory.
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