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...

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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: Wiley 2013-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2013/260156
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author Bert R. Everaert
Vincent J. Nijenhuis
Florence C. M. Reith
Vicky Y. Hoymans
Jean-Pierre Timmermans
Christiaan J. Vrints
author_facet Bert R. Everaert
Vincent J. Nijenhuis
Florence C. M. Reith
Vicky Y. Hoymans
Jean-Pierre Timmermans
Christiaan J. Vrints
author_sort Bert R. Everaert
collection DOAJ
description 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.
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spelling doaj-art-ed11a696bfdf4d59aac4bb6e0aba5ed32025-02-03T06:13:59ZengWileyStem Cells International1687-966X1687-96782013-01-01201310.1155/2013/260156260156Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic CellsBert R. Everaert0Vincent J. Nijenhuis1Florence C. M. Reith2Vicky Y. Hoymans3Jean-Pierre Timmermans4Christiaan J. Vrints5Laboratory of Cell Biology and Histology, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerp, BelgiumLaboratory of Cell Biology and Histology, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerp, BelgiumLaboratory of Cell Biology and Histology, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerp, BelgiumLaboratory of Cellular and Molecular Cardiology, University Hospital Antwerp, Wilrijkstraat 10, 2650 Edegem, BelgiumLaboratory of Cell Biology and Histology, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerp, BelgiumLaboratory of Cellular and Molecular Cardiology, University Hospital Antwerp, Wilrijkstraat 10, 2650 Edegem, BelgiumAim. 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.http://dx.doi.org/10.1155/2013/260156
spellingShingle Bert R. Everaert
Vincent J. Nijenhuis
Florence C. M. Reith
Vicky Y. Hoymans
Jean-Pierre Timmermans
Christiaan J. Vrints
Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
Stem Cells International
title Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
title_full Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
title_fullStr Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
title_full_unstemmed Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
title_short Adiponectin Deficiency Blunts Hypoxia-Induced Mobilization and Homing of Circulating Angiogenic Cells
title_sort adiponectin deficiency blunts hypoxia induced mobilization and homing of circulating angiogenic cells
url http://dx.doi.org/10.1155/2013/260156
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