Circulating endothelial progenitor cells decrease in patients after endarterectomy.
BACKGROUND
Endothelial progenitor cells (EPC) contribute to vascular regeneration. Since surgical injury and burns induce a pro-inflammatory and proangiogenic response, we investigated the effect of vascular injury with minimal surgical trauma after endarterectomy on the number of circulating EPC and systemic inflammatory changes.


RESULTS
Forty-five patients with peripheral arterial occlusive disease were included in the study. Venous blood samples were taken before and 1 day after endarterectomy and plaque material was obtained. Ten patients with minor surgery served as controls. Circulating CD133+CD34+, VEGFR-2+CD34+ progenitor cells and surface expression of CD11b on circulating neutrophils were analysed using flow cytometry. EPCs were characterized in a culture assay as double-positive for DiI-LDL uptake and lectin binding. Cytokine concentrations of interleukin (IL)-6, IL-8, TNF-alpha, IL-1ss, IL-10, IL-12, SDF-1, G-CSF, and VEGF were measured in plasma and tissue samples. After endarterectomy a significant decrease in circulating EPC, CD133+CD34+, and VEGFR-2+CD34+ cells was observed. This was associated with a specific pattern of changes in circulating cytokine levels after endarterectomy with a decrease in IL-1 beta and IL-12, an increase in IL-6 and G-CSF plasma concentrations, and surface expression of CD11b on circulating neutrophils. In contrast, after minor surgery an increase in circulating CD133+CD34+ cells, IL-6, IL-8, and IL-10 was found. Interestingly there was a negative association between levels of local IL-6 within the plaque and only the preoperative levels of circulating CD133+C34+.


CONCLUSIONS
Endarterectomy induces changes in circulating cytokines and a decline in circulating progenitor cells, which may be due to recruitment of progenitor cells to the injured vessels. This is supported by the negative association between plaque inflammation and circulating progenitor cells before endarterectomy.
Stein
Andreas
A
Deutsches Herzzentrum der TU München, München, Germany.
Montens
Hans Peter
HP
Steppich
Birgit
B
Busch
Gabriele
G
Brandl
Richard
R
Ott
Ilka
I
D000071916:AC133 Antigen; D000368:Aged; D015703:Antigens, CD / Q000097:blood; D018952:Antigens, CD34 / Q000097:blood; D001157:Arterial Occlusive Diseases / Q000276:immunology / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D039481:CD11b Antigen / Q000097:blood; D002478:Cells, Cultured; D003251:Constriction, Pathologic; D016207:Cytokines / Q000097:blood; D004691:Endarterectomy; D042783:Endothelial Cells / Q000737:chemistry / Q000276:immunology / Q000473:pathology*; D005260:Female; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D008297:Male; D010455:Peptides / Q000097:blood; D016491:Peripheral Vascular Diseases / Q000276:immunology / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D013234:Stem Cells / Q000737:chemistry / Q000276:immunology / Q000473:pathology*; D013997:Time Factors; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood
D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D039481:CD11b Antigen; D016207:Cytokines; D006023:Glycoproteins; C509295:ITGAM protein, human; C000606023:PROM1 protein, human; D010455:Peptides; D040301:Vascular Endothelial Growth Factor Receptor-2