MYOCD

Official Full Name

myocardin

Organism

Homo sapiens

GeneID

93649

Background

This gene encodes a nuclear protein, which is expressed in heart, aorta, and in smooth muscle cell-containing tissues. It functions as a transcriptional co-activator of serum response factor (SRF) and modulates expression of cardiac and smooth muscle-specific SRF-target genes, and thus may play a crucial role in cardiogenesis and differentiation of the smooth muscle cell lineage. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Sep 2009]

Synonyms

MGBL; MYCD;

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Detailed Information

Myocardin (MYOCD) is a potent transcriptional coactivator that promotes differentiation of myocardium and smooth muscle cells, effectively regulating the proliferation, differentiation and apoptosis of myocardium and smooth muscle cells. In recent years, studies have found that many diseases are associated with abnormal expression of MYOCD genes, such as heart failure, tumors, vascular diseases, and diabetes.

MYOCD Expression Regulation

The CArG sequence located on the promoter of the smooth muscle cells (SMC) marker plays a key role in regulating SMC transcription. The realization of this effect relies on the combination of the serum response factor (SRF) and the CArG box to activate the transcriptional expression of the SMC marker gene. In 2001, Wang et al. isolated and cloned a new SRF helper activator, MYOCD, from a mouse heart cDNA library. It is specifically expressed in embryonic and adult myocardium and SMC and is an essential cofactor in the development and differentiation of heart and SMC. MYOCD binds to SRF through its glutamine-rich domain domain and then forms a MYOCD-SRF-CArG ternary complex with the CArG box to activate the promoters of the myocardium and smooth muscle-specific genes. MYOCD-related transcription factors MRTF-A and MRTF-B have similar structural features and transcriptional activation functions as MYOCD and are widely expressed in tissues and organs. MYOCD, MRTF-A and MRTF-B are commonly referred to as the Myocardin-related transcription factor family.

Figure 1. The model that Myocardin, GSNOR and GSNO created a negative feedback loop to regulate the VSMC phenotypic switch. (Liao, X. H., et al. 2017)

MYOCD and Cardiovascular Disease

As early as 2003, Torrado M first discovered the mRNA level of MYOCD in DCM myocardial tissue. The study found that the expression level of MYOCD mRNA in cardiac muscle tissue of patients with hypertrophic cardiomyopathy and essential hypertension is also increased. Kontaraki JE et al. found that the forced expression of the MYOCD gene in piglets not only reduced the diastolic function of the ventricles, but also affected the electrophysiological activity of cardiomyocytes. Mutation of the 5'-terminal promoter region of the MYOCD gene, which results in down-regulation of the left ventricular function of hypertrophic cardiomyopathy patients. In a rat model of adriamycin-induced heart failure, it was found that silencing MYOCD by short hairpin RNA technology down-regulated the expression of heart failure genes, thereby reducing the degree of impaired cardiac function. A large number of clinical studies and experiments have confirmed that MYOCD expression is increased in a variety of heart diseases, and inhibition or reduction of its expression results in a certain recovery of ventricular function. Therefore, reducing the expression level of MYOCD can be a potential therapeutic target for diseases such as cardiac hypertrophy and heart failure.

MYOCD and Tumor

MYOCD plays a negative growth regulation mechanism in some tumor growth and may be one of the tumor suppressor genes. Studies have shown that MYOCD expression in uterine leiomyosarcoma tissue is reduced. In vitro, the expression of MYOCD significantly inhibited the growth of uterine leiomyosarcoma cells, which was partially achieved by the activation of the growth inhibitor, P21, by the MYOCD-SRF-CArG ternary complex. The study detected a decrease in MYOCD expression in nasopharyngeal carcinoma cells and demonstrated that the inactivation of MYOCD is closely related to the methylation of its promoter. In the experiment, the use of the DNA methylation inhibitor 5-azatoside increased the expression of MYOCD and significantly inhibited the malignant biological behavior of nasopharyngeal carcinoma cells.

References:

Kontaraki, J. E. , Kochiadakis, G. E. , Marketou, M. E. , Chlouverakis, G. , Igoumenidis, N. E. , & Saloustros, I. G. , et al. (2014). Early cardiac gene transcript levels in peripheral blood mononuclear cells reflect severity in stable coronary artery disease. Hellenic J Cardiol, 55(2), 119-125.
Liao, X. H. , Xiang, Y. , Li, H. , Zheng, D. L. , Xu, Y. , & Xi Yu, C. , et al. (2017). Vegf-a stimulates stat3 activity via nitrosylation of myocardin to regulate the expression of vascular smooth muscle cell differentiation markers. Scientific Reports, 7(1), 2660.
Pavneet, S. , Xi-Long, Z. , & Francis, M. . (2014). Dual regulation of myocardin expression by tumor necrosis factor-α in vascular smooth muscle cells. PLoS ONE, 9(11), e112120-.

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