Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells

• Main Authors: Bert R. Everaert, Vincent J. Nijenhuis, Florence C. M. Reith, Vicky Y. Hoymans, Jean-Pierre Timmermans, Christiaan J. Vrints
• Format: Article
• Language: English
• Published: Hindawi Limited 2013-01-01
• Series: Stem Cells International
• Online Access: http://dx.doi.org/10.1155/2013/260156

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.