Abstract:
AIMS:Circulating progenitor cells (PC) may contribute to myocardial recovery following infarction. Growth factors including VEGF are produced during ischaemia and stimulate PC release and activation. In this study, we focused on the functional chemotactic response of PC to VEGF in subjects early after myocardial ischaemia. METHODS AND RESULTS:Number and phenotype of PC were characterized using flow-cytometry. CD133(+)PC were isolated from peripheral blood using positive MACS isolation. The chemotactic response towards members of the VEGF family (VEGF-A, PlGF-1, and VEGF-E) was analysed in three groups: (i) early period following acute myocardial infarction (days 2-4) treated with primary PCI (AMI) (n = 35), (ii) stable coronary artery disease (CAD) (n = 35), and (iii) controls (CTR) (n = 20). CD133(+)PC number was 2-fold higher in AMI when compared with CAD and CTR (P = 0.0001), whereas CAD was not different from CTR. The chemotactic response of CD133(+)PC to VEGF-A, PlGF-1, and VEGF-E was significantly enhanced (2-fold) in AMI when compared with CAD (P = 0.0001). While the increase of the VEGFR-1-mediated/PlGF-triggered response was rapid (2 days following infarction), the VEGFR-2-mediated/VEGF-E-triggered response was maximally increased on day 4 post-AMI, thus correlating with the kinetics of maximal inflammatory activation reflected by increased CRP levels (P = 0.019). CONCLUSION:The enhanced chemotactic response of CD133(+)PC following myocardial infarction represents a novel principle potentially involved in cardiovascular repair early after myocardial infarction. Acute inflammatory processes are closely associated with this increased cellular function.
journal_name
Eur Heart Jjournal_title
European heart journalauthors
Vöö S,Eggermann J,Dunaeva M,Ramakers-van Oosterhoud C,Waltenberger Jdoi
10.1093/eurheartj/ehm542subject
Has Abstractpub_date
2008-01-01 00:00:00pages
241-50issue
2eissn
0195-668Xissn
1522-9645pii
ehm542journal_volume
29pub_type
杂志文章abstract::Recent studies have illustrated that in addition to the well known risk factors, such as lipoproteins, smoking, hypertension, there are others that cause atherosclerosis and myocardial infarction. Our knowledge of atherosclerotic lesions has increased. We now know that atherosclerotic changes are due to inflammatory c...
journal_title:European heart journal
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