Adiponectin deficiency blunts hypoxia-induced mobilization and homing of circulating angiogenic cells
Faculty of Medicine and Health Sciences
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Stem Cells International
, p. 1-8
University of Antwerp
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.