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.