Adiponectin deficiency blunts hypoxia-induced mobilization and homing of circulating angiogenic cells.

Aim. We investigated the effects of adiponectin deficiency on circulating angiogenic cell (CAC) mobilization, homing, and neovascularization in the setting of acute myocardial infarction (AMI). Methods & Results. AMI was induced in wild-type (WT) (n = 10) and adiponectin knockout (Adipoq (-/-)) mice (n = 7). One week after AMI, bone marrow (BM) concentration and mobilization of Sca-1(+) and Lin(-)Sca-1(+) progenitor cells (PCs) were markedly attenuated under Adipoq (-/-) conditions, as assessed by flow cytometry. The mRNA expression of HIF-1-dependent chemotactic factors, such as Cxcl12 (P = 0.005) and Ccl5 (P = 0.025), and vascular adhesion molecules, such as Icam1 (P = 0.010), and Vcam1 (P = 0.014), was significantly lower in the infarction border zone of Adipoq (-/-) mice. Histologically, Adipoq (-/-) mice evidenced a decrease in neovascularization capacity in the infarction border zone (P < 0.001). Overall, capillary density was positively correlated with Sca-1(+) PC numbers in BM (P = 0.01) and peripheral blood (PB) (P = 0.005) and with the expression of the homing factors Cxcl12 (P = 0.013), Icam1 (P = 0.034) and Vcam1 (P = 0.014). Conclusions. Adiponectin deficiency reduced the BM reserve and mobilization capacity of CACs, attenuated the expression of hypoxia-induced chemokines and vascular adhesion molecules, and impaired the neovascularization capacity one week after AMI.