Endothelial progenitor cell number and colony-forming capacity in overweight and obese adults

Abstract

ObjectiveTo investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity.DesignCross-sectional study of normal weight, overweight and obese adult humans.SubjectsSixty-seven sedentary adults (age 45–65y): 25 normal weight (BMI ≤ 25 kg/m2; 12 males/13 females); 18 overweight (BMI = 25–29.9 kg/m2; 12 males/6 females); and 24 obese (BMI ≥ 30 kg/m2; 18 males/6 females). All subjects were non-smokers and free of overt cardiometabolic disease.MeasurementsPeripheral blood samples were collected and circulating EPC number was assessed by flow cytometry. Putative EPCs were defined as CD45−/CD34+/VEGFR-2+/CD133+ or CD45−/CD34+ cells. EPC colony-forming capacity was measured in vitro using a colony-forming unit assay.ResultsNumber of circulating putative EPCs (either CD45−/CD34+/VEGFR-2+/CD133+ or CD45−/CD34+ cells) was lower (P<0.05) in obese (0.0007±0.0001%; 0.050±0.006%) compared with overweight (0.0016±0.0004%; 0.089±0.019%) and normal weight (0.0015±0.0003%; 0.082±0.008%) adults. There were no differences in EPC number between the overweight and normal weight groups. EPC colony-formation was significantly less in the obese (6±1) and overweight (4±1) compared with normal weight (9±2) adults.ConclusionThese results indicate that: 1) the number of circulating EPCs is lower in obese compared with overweight and normal weight adults; and 2) EPC colony-forming capacity is blunted in overweight and obese adults compared with normal weight adults. Impairments in EPC number and function may contribute to adiposity-related cardiovascular risk.

Reduction of both number and proliferative activity of human endothelial progenitor cells in obesity

“…Endothelial progenitor cells in obesity K Tobler et al the best of our knowledge, the relation of circulating EPCs to ApoB, lipoprotein (a) and plasma free fatty acids has not been previously studied in detail. However, in accordance with our data, cholesterol [14][15][16] and triglycerides 14,16 were already described to be ineffective on CD34 þ /KDR þ and CD45 À /CD34 þ /VEGFR-2 þ /CD133 þ EPCs, whereas heterogeneous results were found on the effects of LDL on EPC numbers. 14,16,17 Although there are several reports on reduced EPCs in diabetes, 15,16 little attention has been paid to a direct association between EPCs and glycosylated hemoglobin.…”

“…Thereby, the results of our study extend reports of reduced CD34 þ /KDR þ EPCs (1) in obese men with metabolic syndrome compared with lean and healthy controls 12 and (2) in participants of a weight loss study before and after their attendance at a diet program, 13 as well as (3) of a decreased number of CD45 À / CD34 þ /VEGFR-2 þ /CD133 þ EPCs in a small study group of obese adults. 14 Although the number of all subsets of EPCsFdefined as cells coexpressing CD133 and/or CD34 in combination with the endothelial surface marker KDRFnegatively correlates with BMI, CPCs (defined as CD34 þ /CD133 þ double-positive cells) are not affected by obesity (data not shown). The latter finding is, however, in contrast to one of the previous studies reporting reduced numbers of CD34 þ /CD133 þ CPCs with increasing BMI, 13 although the reason for this discrepancy remains elusive.…”

“…So far, the investigation of EPC number in relation to hsCRP or hypertension led to heterogeneous results. [14][15][16][18][19][20] However, for determination of extremely rare eventsFas is the case in EPC analysisFa very high number of PBMCs must be analyzed to obtain reliable results. As an aside, we had the possibility to evaluate about 30-50 times more events in this study compared with most of the previous reports.…”

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

“…They contribute to endothelial repair by attracting circulating EPC in the blood and by stimulating their integration into the injured endothelium via the secretion of angiogenic growth factors. Obese adults have reduced and dysfunctional CAC (78). In obese children, CAC are also functionally defective (79), thereby shifting the balance in these children even further towards higher endothelial damage and reduced repair capacity (Figure 2).…”

Endothelial progenitor cells in overweight: exhausted long before the summit?

“…With great interest, we read the article by MacEneaney et al 1 that was published very recently in this journal. The authors showed in a well-designed study the influence of overweight and obesity on endothelial progenitor cells (EPCs) in adults.…”