Tie2 lineage deletion of 6 integrin: endothelial and haematopoietic cells in neovascularization

Abstract

This editorial refers to ‘Tie2-dependent knockout of α6 integrin subunit in mice reduces post-ischaemic angiogenesis’ by C. Bouvard et al ., pp. 39–47, this issue. The metabolic demand of a mature tissue determines the degree of blood and oxygen supply, which normally is controlled by vasoregulation at the level of arteriolar resistance vessels. However, in specific conditions such as inflammation and excessive tissue growth including tumours, the metabolic demand exceeds the supply by autoregulation and therefore requires neovascularization. The need for additional blood supply and neovascularization becomes urgent after an acute vascular occlusion. Rapid formation of collaterals is then required, while the distal hypoxic tissue simultaneously shifts to the production of pro-angiogenic factors, in particular vascular endothelial growth factor, which subsequently induces sprouting angiogenesis in an attempt to connect to other perfused vessels and to restore oxygen and nutrient supply to the ischaemic tissue. In addition, circulating monocytes and endothelial progenitor cells (EPCs) are recruited to the sites of structural arterial widening (arteriogenesis) and sprouting angiogenesis. Monocytes and circulating angiogenic cells (monocyte-lineage cells that acquire several endothelial markers, also called early outgrowth EPCs) support the vascular adaptation in a paracrine manner.1 Furthermore, endothelial colony-forming cells (ECFCs, also called late outgrowth EPCs), which are present in small numbers …