MEOX2

Official Full Name

mesenchyme homeobox 2

Organism

Homo sapiens

GeneID

4223

Background

This gene encodes a member of a subfamily of non-clustered, diverged, antennapedia-like homeobox-containing genes. The encoded protein may play a role in the regulation of vertebrate limb myogenesis. Mutations in the related mouse protein may be associated with craniofacial and/or skeletal abnormalities, in addition to neurovascular dysfunction observed in Alzheimer's disease. [provided by RefSeq, Jul 2008]

Synonyms

GAX; MOX2;

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Detailed Information

In mammalian cells, the homeobox gene is divided into two major categories: the Hox gene and the heterogeneous Hox gene. The Hox gene is further divided into A, B, C, and D 4 families, and the heterogeneous Hox gene contains Meox, P ax, En. And other families. The heterozygous Hox gene plays an important role in the development of the posterior half of the higher body and the development of certain organs. Among them, Meox2 (M esoderm homeobox2) in the Meox family is involved in the negative regulation of vascular smooth muscle cells (VSMC) and cardiomyocyte cycle, and plays a role in the development of the cardiovascular system.

At different stages of mouse embryonic development, Meox2 expression was detected in the smooth muscle of the hindgut, the stomach, the posterior pharynx, the esophagus, the diaphragm, the smooth muscle of the bladder, and in the vasculature including the thymus and kidney. Meox2 is expressed in the aorta, vascular, saphenous vein, and vascular smooth muscle of the internal mammary artery in adults. In various tissues of adult rabbits, Meox2 is mainly expressed in the cardiovascular system. Compared with the expression levels of heart and other tissues, Meoox2 has the highest expression level in the descending thoracic aorta. Meox1 knockout mice have rib and vertebra fusion, but Meox2 knockout mice have defects in limb muscle development. Mice that knocked out Meox1 and Meox2 simultaneously showed a more severe phenotype, and most of the skeletal and midshaft bones could not form. This indicates that the Meox gene is essential for the normal development of the embryo.

Figure 1. Model of the signaling pathway for Ski modulation of myofibroblast phenotype.（Cunnington, R. H. , et al. 2014）

Meox2 and Vascular Smooth Muscle Cells

Platelet-derived growth factor (PDGF) and growth factors regulate the proliferation and differentiation of vascular smooth muscle cells (VSMC). VSMCs were isolated from rabbit aorta and cultured for 3 days in the absence of plasma, leaving them at rest. The VSMC was then stimulated by the addition of feta l bovine serum (FCS) or PDGF (as mitogen), and the mRNA level of Meox2 was rapidly down-regulated. Meox2 expression levels began to recover at 24 h after stimulation and returned to baseline levels 24 to 48 h after stimulation. After rapid growth of VSMC, cells were cultured in serum-free medium and the expression level of Meox2 increased five-fold within 24 h. These results indicate that Meox2 may have a function of regulation of G0/G1 conversion in the VSMC cycle. Other studies have shown that Meox2 has a significant correlation with the inhibition of VSM C proliferation after angioplasty and the up-regulation of cyclin-dependent kinase inhibitor (p21C IPI) expression. The inhibition of VSMC proliferation by Meox2 transitional expression is mediated by p21C IPI.

Meox2 and Angiogenesis

The regulation of vascular endothelial cells by Meox2 was studied. Northern blot, PCR, and cellular immunohistochemistry were used to detect the expression of Meox2 in normal vascular endothelial cells. Meox2 gene was transfected into umbilical vein endothelial cells (HUVEC) by replication-deficient adenovirus. The investigators then determined the proliferation of HUVEC, the uptake of 3H-thymidine, the expression of p21, and the formation of blood vessels after infection with different doses of virus. It was found that Meox2 strongly inhibited the proliferation of HUVEC, and the uptake of 3H-thymidine was also strongly inhibited by mitogen stimulation. Northern blot analysis revealed that the expression of p21 was up-regulated by 5 fold, the activity of the p21 promoter was activated 4 to 5 times, and the formation of blood vessels was significantly inhibited.

References:

G Cunnington, R. H. , Northcott, J. M. , Ghavami, S. , Filomeno, K. L. , Jahan, F. , & Kavosh, M. S. , et al. (2014). The ski-zeb2-meox2 pathway provides a novel mechanism for regulation of the cardiac myofibroblast phenotype. Journal of Cell Science,127(1), 40-49.
Northcott, J. M. , Czubryt, M. P. , & Wigle, J. T. . (2017). Vascular senescence and ageing: a role for the meox proteins in promoting endothelial dysfunction 1. Canadian Journal of Physiology & Pharmacology, 95(10).
Tian, L. , Tao, Z. Z. , Ye, H. P. , Li, G. Y. , Zhan, Z. F. , & Tuo, H. W. . (2018). Over-expression of meox2 promotes apoptosis through inhibiting pi3k/akt pathway in laryngeal cancer cells. Neoplasma.

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