Up-regulation of VE-cadherin expression by the LMO2 complex promotes vascular remodeling

LMO2 and its binding partner TAL1/SCL have essential roles in both hematopoiesis and angiogenesis. Indeed, LMO2 is highly expressed in endothelial cells and hematopoietic stem cells (HSCs) almost exclusively (with exceptions) throughout life. Recently, the first birthplace of HSCs has been identified as hemogenic endothelial cells in the dorsal aorta in mammals. Firstly, the LMO2 complex including TAL1, GATA1/2/3 (i.e., GATA1 or GATA2 or GATA3), and LDB1 play a key role in endothelial to hemogenic endothelial cell transition in the dorsal aorta in producing HSCs. Another role of the LMO2 complex is to remodel the existing vascular system in angiogenesis. In 2007 and 2012, progress was made in dissecting the mechanism of vascular remodeling regulated by the LMO2 complex. Two of the pivotal role players in vascular remodeling, VE-cadherin and angiopoitin-2, were identified to be among the direct targets of the LMO2 transcription factor complex. In this review, the detailed mechanism in vascular remodeling via the LMO2 complex is discussed