Abstract
The SRY (Sex Determining Region Y)-related HMG box of DNA binding proteins, referred to as SOX transcription factors, were first identified as critical regulators of male sex determination but are now known to play an important role in vascular development and disease. SOX7, 17, and 18 are essential in endothelial differentiation and SOX2 has emerged as an essential mediator of endothelial-mesenchymal transitions (EndMTs), a mechanism that enables the endothelium to contribute cells with abnormal cell differentiation to vascular disease such as calcific vasculopathy. In the following paper, we review published information on the SOX transcription factors in endothelial differentiation and hypothesize that SOX2 acts as a mediator of EndMTs that contribute to vascular calcification.
Highlights
Appropriate endothelial cell (EC) differentiation is essential to support vascularization of tissues and maintain proper vascular homeostasis
We found ECs that were double positive for the endothelial marker fetal liver kinase 1 (Flk1) and SOX2 adjacent to differentiating brain cells on E10.5 and E14 [49]
We found that the Sox2 depletion delayed the endothelial marker induction and changed the temporal sequence of neuronal and endothelial differentiation (Figure 2A)
Summary
Appropriate endothelial cell (EC) differentiation is essential to support vascularization of tissues and maintain proper vascular homeostasis. In coordination with tissue development, ECs are derived from progenitor cells that undergo endothelial lineage differentiation to form functional vascular networks [1, 2]. EndMTs have been revealed as novel sources of calcifying cells for vascular calcification, which is considered to be a form of ectopic bone formation and involves multipotent cells and networks of growth factors and transcription factors [10]. We review the SOX factors in endothelial differentiation and EndMTs and include some of our results to support previous studies. We briefly review the SOX factors in EndMTs, and argue that SOX2 induces EndMTs and serves as a novel cellular source in vascular calcification
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