Disease relevance of Meox2

• These results suggest that Gax is a common transcription factor involved in the signaling pathway of vascular growth for Ang II and CNP and regulates the cell cycle and/or phenotype of VSMCs for vascular remodeling in hypertension and atherosclerosis [1].
• Gax also inhibits the proliferation of vascular smooth muscle cells when overexpressed with a replication-defective adenovirus vector, and the local delivery of this recombinant virus to denuded rat carotid arteries significantly reduces neointima formation and luminal narrowing [2].

High impact information on Meox2

• The homeobox transcription factor Gax is expressed in quiescent vascular smooth muscle cells (VSMCs), and its expression is downregulated by vascular injury or other conditions that lead to VSMC proliferation [3].
• Flow cytometric analysis implicated a Gax-mediated downregulation of alpha(v)beta(3) and alpha(v)beta(5) integrin expression in VSMCs as a potential cause for reduced cell motility [3].
• Regulation of smooth muscle cell migration and integrin expression by the Gax transcription factor [3].
• These data suggest that Gax is likely to have a regulatory function in the G0-to-G1 transition of the cell cycle in vascular smooth muscle cells [4].
• Adenovirus-mediated delivery of the Gax transcription factor to rat carotid arteries inhibits smooth muscle proliferation and induces apoptosis [5].

Biological context of Meox2

• The Gax down-regulation is dose dependent and can be correlated with the mitogen's ability to stimulate DNA synthesis [4].
• We further examined the involvement of mitogen-activated protein kinases (MAPKs), which is crucial for cell growth and has shown to be activated by oxidative stress, on the regulation of Gax expression by Ang II [6].
• These data suggest that deregulated Gax expression induces first cell cycle arrest and then apoptosis in the vascular smooth muscle cells that contribute to the neointimal layer [5].
• Opposite regulation of Gax homeobox expression by angiotensin II and C-type natriuretic peptide [1].
• In the present study, we examined the effects of Ang II and CNP on Gax gene expression in VSMCs [1].

Anatomical context of Meox2

• PDGF-AA, a weak mitogen for rat vascular smooth muscle cells, did not affect Gax transcript levels, while PDGF-AB and -BB, potent mitogens for these cells, were nearly as effective as fetal bovine serum [4].
• Currently we are performing percutaneous Gax adenovirus-mediated gene transfer into normal and atherosclerotic rabbit iliac arteries [2].

Associations of Meox2 with chemical compounds

• We previously reported that Ang II down-regulated Gax expression [6].
• Ang II and H2O2 decreased Gax expression dose-dependently and these effects were blocked by administration of both NAC and pyrrolidine dithiocarbamate (PDTC), another anti-oxidant [6].
• Ang II- or H2O2 -induced Gax down-regulation was significantly inhibited by PD98059, an ERK1/2 inhibitor but not SB203580, a p38MAPK inhibitor [6].

References