Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
| Autor: | Vicky Y. Hoymans, Christiaan J. Vrints, Vincent J. Nijenhuis, Florence C. M. Reith, Jean-Pierre Timmermans, Bert R Everaert |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
Chemokine lcsh:Internal medicine Article Subject CCL5 Neovascularization Internal medicine Medicine Progenitor cell lcsh:RC31-1245 Molecular Biology Biology Adiponectin biology business.industry Cell adhesion molecule Cell Biology medicine.anatomical_structure Endocrinology Immunology biology.protein Bone marrow Human medicine medicine.symptom business Homing (hematopoietic) Research Article |
| Zdroj: | Stem Cells International, Vol 2013 (2013) Stem Cells International |
| ISSN: | 1687-966X |
| DOI: | 10.1155/2013/260156 |
| Popis: | 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 underAdipoq−/−conditions, as assessed by flow cytometry. The mRNA expression of HIF-1-dependent chemotactic factors, such asCxcl12(P=0.005) andCcl5(P=0.025), and vascular adhesion molecules, such asIcam1(P=0.010), andVcam1(P=0.014), was significantly lower in the infarction border zone ofAdipoq−/−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 factorsCxcl12(P=0.013),Icam1(P=0.034) andVcam1(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. |
| Databáze: | OpenAIRE |
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