MEF2A

Official Full Name

myocyte enhancer factor 2A

Organism

Homo sapiens

GeneID

4205

Background

The protein encoded by this gene is a DNA-binding transcription factor that activates many muscle-specific, growth factor-induced, and stress-induced genes. The encoded protein can act as a homodimer or as a heterodimer and is involved in several cellular processes, including muscle development, neuronal differentiation, cell growth control, and apoptosis. Defects in this gene could be a cause of autosomal dominant coronary artery disease 1 with myocardial infarction (ADCAD1). Several transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Jan 2010]

Synonyms

mef2; ADCAD1; RSRFC4; RSRFC9;

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Detailed Information

MEF2A is a member of the transcription factor myocyte enhancer factor 2 (MEF2) family. In the spinal animal, the myocyte enhancer factor 2 family members include four transcription factors, MEF2A, MEF2B, MEF2C, and MEF2D. The MEF2A protein is a class of deoxyribonucleic acid (DNA) binding proteins that have many unique functionalities. They bind to specific sequences in the gene promoter, thereby regulating gene expression.

The Role of MEF2A

MEF2A has a variety of regulatory modes including fine adjustments suitable for developmental processes, and its binding sites are widely present in specific gene regulatory regions of muscle and endothelium. MEF2A is expressed in the cardiovascular system, lymphoid immune system, respiratory system, adipose tissue and endothelial tissue. The most prominent function is to control gene transcription during myocyte differentiation, mediate cell differentiation during skeletal muscle, myocardium and smooth muscle development, and participate in vascular development.

Figure 1. Mechanisms of MEF2A in regulating myogenesis of bovine skeletal muscle primary myoblasts. (Ya-Ning, W. , et al. 2018)

In addition, MEF2A can also be combined with a variety of regulatory factors to activate a gene that does not have a MEF2A site. The expression of MEF2A affects heart development and can lead to cardiac remodeling. The tissue specificity and significance of MEF2A expression is similar to vascular endothelial growth factor receptor 2 (VEGFER 2) and von Willebrand factor in endothelium progenitor cells. Studies have shown that MEF2A can serve as an early marker of angiogenesis and may play an important role in controlling angiogenesis.

MEF2A and Vascular Inflammation

Studies have shown that chemokines linked to inflammation play an important role in the development, progression and evolution of atherosclerosis. Studies have shown that MEF2A mediates vascular inflammation via the p38 mitogen-activated protein kinases (MAPK) pathway. Mitogen-activated protein kinase 1 is another MAPK pathway that regulates the function and proliferation of vascular endothelial cells by altering the transcriptional activity of MEF2A. In addition, cyclooxygenase-2 (COX-2) expressed by macrophages or other cells promotes prostaglandin synthesis at the site of inflammation and causes an inflammatory reaction with proteases and other mediators. However, studies have confirmed that nuclear respiratory factor-1 (NRF-1) can induce the expression of MEF2A mRNA, which allows the MEF2A protein to coordinate the respiratory chain subunits expression in the myocardium through the NRF-1-MEF2A-COX transcriptional cascade. Mutations in the MEF2A gene may alter the MAPK pathway and increase COX-2 expression, thereby accelerating the progression of vascular inflammation and promoting apoptosis and shedding of vascular endothelial cells, which results in easier adhesion and infiltration of monocytes into the vascular endothelium.

MEF2A and Coronary Heart Disease

The established MEF2A-deficient mouse model was used to study the effect of MEF2A on the differentiation of vascular smooth muscle cells. It was found that the expression of MEF2A gene was found in mouse cardiomyocytes after birth. Most mice lacking MEF2A die within one week of birth, and their right ventricle enlarges, muscle fibers rupture, and mitochondria disintegrate. A small number of MEF2A-deficient mice are prone to sudden death due to myocardial mitochondrial dysfunction even if they survive to adulthood. Their results suggest that MEF2A plays an important role in maintaining proper mitochondrial function and structural integrity of cardiomyocytes. Studies have shown that immunofluorescence staining and PCR have detected MEF2A expression in coronary endothelial cells. Therefore, MEF2A can be considered to play an important role in endothelial development and function.

References:

Ya-Ning, W. , Wu-Cai, Y. , Pei-Wei, L. , Hong-Bao, W. , Ying-Ying, Z. , & Lin-Sen, Z. , et al. (2018). Myocyte enhancer factor 2a promotes proliferation and its inhibition attenuates myogenic differentiation via myozenin 2 in bovine skeletal muscle myoblast. PLOS ONE, 13(4), e0196255-.
Pon, J. R. , & Marra, M. A. . (2016). Mef2 transcription factors: developmental regulators and emerging cancer genes. Oncotarget, 7(3), 2297-2312.
Eros, D. G. , Hancock, W. W. , & Claudio, B. . (2018). Mef2 and the tumorigenic process, hic sunt leones. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, S0304419X18300702-.

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