MEOX1

Official Full Name

mesenchyme homeobox 1

Organism

Homo sapiens

GeneID

4222

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 molecular signaling network regulating somite development. Alternatively spliced transcript variants encoding different isoforms have been described. [provided by RefSeq, Jul 2008]

Synonyms

KFS2; MOX1;

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Detailed Information

The mesoderm/mesenchyme homeobox gene (Meox) belongs to the Homeobox gene (Hox). Homeobox genes are expressed in almost all eukaryotes, with 11 gene types in animals, more than 100 gene families, and 14 gene types in plants. The Meox gene is a member of a subfamily of homeobox genes that are expressed in mesoderm and mesenchyme, and the encoded protein may regulate somatic development. The Meox family has two members, including Meox1 and Meox2, and 98% of the amino acid sequences are identical. The difference between the two sequences is mainly outside the highly conserved region.

In the primitive stage of embryonic development, Meox1 forms mesodermal expression in the original head and heart in the future, rather than in the ectoderm and endoderm of neural tissue. Thus, mesodermal/mesomeric homeobox genes form mesoderm and neuroectoderm before or at the initial stage, and Meox1 expression may have revealed a broad "post-path" domain of embryonic mesoderm. In the newly formed somites, the expression of Meox1 is expressed throughout the somites of the skeletal and dermatomes, and when the body is segmented, Meox1 is restricted to the expression of the dermatomes. Skeletal muscle growth is driven by stem cells, which have extensive clonal drift. The homeobox gene meox1 controls clonal drift during muscle growth.

Figure 1. The homeobox gene meox1 controls clonal drift during muscle growth. (Nguyen, P. D., et al. 2017)

Meox1 Regulation of Cardiovascular System

To investigate the role of Meox1 in the differentiation of smooth muscle cells, it was found that transforming growth factor-β induces Meox1 expression in the initial stage of smooth muscle cell differentiation of pluripotent mesenchymal C3H10T1 /2 cells. Moreover, specific inhibitors block both PI3K and Smad3 signaling pathways, resulting in decreased expression of Meox1 and smooth muscle cell markers. Importantly, knockdown of Meox1 by specific shRNA inhibited TGF-β-induced expression of early markers of smooth muscle cells, including SM22α and calponin. On the other hand, Meox1 overexpression increases smooth muscle cell marker expression. These results indicate that Meox1 is a novel regulator of TGF-β-induced smooth muscle cell differentiation.

After the Meox1 gene was transfected into chick embryos at an early developmental stage for several hours, it was found to affect the division of cardiomyocytes in the early cardiac cyclization phase and inhibit cardiomyocyte proliferation. This study suggests that Meox1 may negatively regulate the proliferation of cardiomyocytes, and premature expression of homeobox genes in embryonic heart development may lead to normal morphogenesis in the heart. Overexpression of Meox1 in the heart of transgenic mice leads to dilated cardiomyopathy, suggesting that Meox1 may be one of the modified genes that enhance the pathogenesis of cardiomyopathy.

Regulation of Cardiac Fibroblasts by Meox1

The study found that Meox1 does not affect phenotypic changes in fibroblasts and myofibroblasts. The study found that Meox1 is expressed in the interstitial fibrosis region of heart failure, and Meox1 is expressed in vitro and in vivo with limited expression of cardiac fibroblasts. Paracrine signals from cardiomyocytes can increase Meox1-positive fibroblasts, and Meox1 knockdown completely inhibits reactive proliferation of cardiac fibroblasts. Gene expression indicated that knockdown of Meox1 resulted in down-regulation of mitosis-related gene expression. In fact, Meox1 knockdown reduces mitotic cells, which in turn increases the proportion of DNA-synthesized cells, thereby inhibiting the transition of mitosis. Synchronous cell cycle analysis and promoter analysis using live cell imaging indicated that Meox1 oscillated throughout the cell cycle and specifically appeared in the G2/M phase. Meox1, which is heterologously expressed in interstitial fibrosis, is derived from ventricular heart tissue in patients with end-stage heart failure. It is noteworthy that Meox1 expression is significantly associated with fibrosis-associated genes in diseased ventricular tissues, indicating pathological relevance in the clinical setting.

References:

Nguyen, P. D. , Gurevich, D. B. , Sonntag, C. , Hersey, L. , Alaei, S. , & Nim, H. T. , et al. (2017). Muscle stem cells undergo extensive clonal drift during tissue growth via meox1-mediated induction of g2 cell-cycle arrest. Cell Stem Cell, 21(1), 107-119.e6.
Dauer, M. V. P. , Currie, P. D. , & Berger, J. . (2018). Skeletal malformations of meox1-deficient zebrafish resemble human klippel-feil syndrome. Journal of Anatomy.
Lu, D. , Wang, J. , Li, J. , Guan, F. , Zhang, X. , & Dong, W. , et al. (2017). Meox1 accelerates myocardial hypertrophic decompensation through gata4. Cardiovascular Research.

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