The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.

Waspe, Lawrence E.; Ordahl, Charles P.; Simpson, Paul C.

doi:10.1172/jci114554

Cited by 182 publications

(102 citation statements)

References 58 publications

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“…Cell Culture and Transfection-Neonatal rat ventricular myocytes (NRVMs) were prepared according to the method described in Waspe et al (28). Briefly, 150,000 cells/well were plated in 12-well tissue culture plates coated with gelatin.…”

Section: Methodsmentioning

confidence: 99%

Yin Yang 1 Is Increased in Human Heart Failure and Represses the Activity of the Human α-Myosin Heavy Chain Promoter

Sucharov

Mariner

Long

et al. 2003

Journal of Biological Chemistry

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Yin Yang 1 (YY1) is a transcription factor that can repress or activate transcription of the genes with which it interacts. In this report we show that YY1 is a negative regulator of the ␣-myosin heavy chain (␣MyHC) gene, which, with ␤MyHC are the molecular motors of the heart. ␣MyHC mRNA and protein levels are downregulated in hypertrophy and heart failure, and this is thought to be detrimental for cardiac contractility. We show that YY1 specifically interacts with the ␣MyHC promoter and that overexpression of YY1 in cardiac cells represses the activity of the ␣MyHC promoter. We also show that the 170 -200-amino acid region of YY1, important for its interaction with histone acetyl transferases and histone deacetylases, is important for its repressive activity and that YY1 deleted in this region is an activator of the ␣MyHC promoter. Moreover, we show that YY1 levels and DNA binding activity are increased in failing human left ventricles and in a mouse model of hypertrophic cardiomyopathy, where ␣MyHC levels are decreased. These results suggest that YY1 is a negative regulator of ␣MyHC gene expression.

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Section: Methodsmentioning

confidence: 99%

Yin Yang 1 Is Increased in Human Heart Failure and Represses the Activity of the Human α-Myosin Heavy Chain Promoter

Sucharov

Mariner

Long

et al. 2003

Journal of Biological Chemistry

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show abstract

“…Finally, by use of primary cultures of cardiac myocytes, it was demonstrated that adenylate cyclase activators and cAMP analogues activate the expression of the αMHC isoform (V1) and the αMHC mRNA transcript [66,67]. The α1-adrenergic agonists or activators of the PK-c pathway, on the other hand, led to increased expression of the V3 myosin isoform and a relative abundance of βMHC mRNA [66,67,76]. However, in an earlier study using cultures of cardiac myocytes grown in a serum-free defined medium, no effect of either β-or α-adrenergic agonists on the expression MHC mRNA was found [77].…”

Section: Role Of Adrenergic Stimulationmentioning

confidence: 99%

Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure

Gupta

2007

Journal of Molecular and Cellular Cardiology

186

171

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“…This finding may be because these genes are exquisitely regulated in vivo by extrinsic factors such as circulatory levels of thyroid hormone and catecholamines, in addition to neuronal input, all of which are difficult to accurately reproduce in cell culture (Waspe et al, 1990;Flink et al, 1992;Kariya et al, 1994). In addition, the ␣ MyHC gene promoter exhibited distinct behavior in vivo when analyzed by direct DNA injection compared with the regulation observed in transgenic mice (Subramaniam et al, 1991;Buttrick et al, 1993).…”

Section: Interplay Between An Upstream Cardiac-enhancer and Proximal mentioning

confidence: 99%

In vivo regulation of the chicken cardiac troponin T gene promoter in zebrafish embryos

Tidyman

Sehnert

Huq

et al. 2003

Developmental Dynamics

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The chicken cardiac troponin T (cTnT) gene is representative of numerous cardiac and skeletal muscle-specific genes that contain muscle-CAT (MCAT) elements within their promoters. We examined the regulation of the chicken cTnT gene in vivo in zebrafish embryos, and in vitro in cardiomyocyte, myoblast, and fibroblast cultures. Defined regions of the cTnT promoter were linked to the green fluorescent protein (GFP) gene for in vivo analysis, and the luciferase gene for in vitro analysis. Injection of the cTnT promoter constructs into fertilized zebrafish eggs resulted in GFP expression in both heart and skeletal muscle cells reproducing the pattern of expression of the endogenous cTnT gene in the chicken embryo. Promoter deletion analysis revealed that the cis-regulatory regions responsible for cardiac and skeletal muscle-specific expression functioned in an equivalent manner in both in vitro and in vivo environments. In addition, we show that mutation of the poly-ADP ribose polymerase-I (PARP-I) binding site adjacent to the distal MCAT element in the chicken cTnT promoter produced a non-cell-specific promoter in vitro and in the zebrafish. Thus, the PARP-I transcriptional regulatory mechanism that governs muscle specificity of the chicken cTnT promoter is conserved across several chordate classes spanning at least 350 million years of evolution.

show abstract

The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.

Cited by 182 publications

References 58 publications

Yin Yang 1 Is Increased in Human Heart Failure and Represses the Activity of the Human α-Myosin Heavy Chain Promoter

Yin Yang 1 Is Increased in Human Heart Failure and Represses the Activity of the Human α-Myosin Heavy Chain Promoter

Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure

In vivo regulation of the chicken cardiac troponin T gene promoter in zebrafish embryos

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