Aging, exercise, and endothelial progenitor cell clonogenic and migratory capacity in men

Abstract

Numerical and functional impairment of circulating endothelial progenitor cells (EPCs) is thought to contribute to vascular aging and the associated increase in cardiovascular risk. We tested the following hypotheses: 1) EPC clonogenic and migratory capacity decrease progressively with age in healthy, sedentary adult men; and 2) regular aerobic exercise will improve EPC clonogenic and migratory capacity in previously sedentary middle-aged and older men. Peripheral blood samples were collected from 46 healthy sedentary men: 10 young (26 +/- 1 yr), 15 middle-aged (47 +/- 1 yr), and 21 older (63 +/- 1 yr). Mononuclear cells were isolated and preplated for 2 days, and nonadherent cells were further cultured for 7 days to determine EPC colony-forming units. Migratory activity of EPCs was determined using a modified Boyden chamber. Ten sedentary middle-aged and older men (59 +/- 3 yr) were studied before and after a 3-mo aerobic exercise intervention. The number of EPC colony-forming units was approximately 75% lower (P < 0.01) in middle-aged (12 +/- 3) and older (8 +/- 2) compared with young (40 +/- 7) men. There was no difference in colony count between middle-aged and older men. EPC migration (fluorescent units) was significantly reduced in older (453 +/- 72) compared with young (813 +/- 114) and middle-aged (760 +/- 114) men. The exercise intervention increased (P < 0.05) both EPC colony-forming units (10 +/- 3 to 22 +/- 5) and migratory activity (683 +/- 96 to 1,022 +/- 123) in previously sedentary middle-aged and older men. These results provide further evidence that aging adversely affects EPC function. Regular aerobic-endurance exercise, however, is an effective lifestyle intervention strategy for improving EPC clonogenic and migratory capacity in middle-aged and older healthy men.

Human aging and CD31+T-cell number, migration, apoptotic susceptibility, and telomere length

“…In contrast to CD31 ϩ T-cell number, migratory capacity declined precipitously from the young to the middleaged men and was not different between the middle-aged and older men. This temporal pattern is similar to that previously reported for endothelial progenitor cells (19), supporting the notion that CD31 ϩ T cells comprise part of the circulating vascular progenitor milieu (20). Reduced migratory capacity of circulating CD31 ϩ T cells with age may seriously compromise vascular repair processes and contribute to poor clinical outcomes (13).…”

“…The migratory capacity of CD31 ϩ T cells was assessed using a modified Boyden chamber technique, as previously described by our laboratory (19). Briefly, 4 ϫ 10 5 cells were resuspended in culture medium consisting of RPMI 1640 (CellGro; Mediatech, Manassas, VA), penicillin (100 U/ml), and streptomycin (100 g/ml) and then placed in the upper buffer chamber of a 24-well modified Boyden chamber coated with fibronectin (FluoroBok; BD Biosciences).…”

“…Diminished endogenous repair capacity is believed to contribute to the etiology of atherosclerotic disease with advancing age (13,19). Indeed, decreased bioavailability and/or function of reparative factors is linked with a number of age-related pathologies, such as hypertension, diabetes, and obesity (1,28,35).…”

Endothelial progenitor cells: Implications for cardiovascular disease

“…The importance of NO for the exercise-induced release of EPCs was supported by the analysis of eNOS knockout mice. These results could be confirmed by several other groups investigating patients with coronary artery disease (74), peripheral vascular occlusive disease (9), chronic heart failure (75), hemodialysis (76), or even health controls (77,78). Even in school children, a recent study from our group confirmed the impact of exercise on EPCs (79).…”

O grau de melhora na função das células progenitoras endoteliais derivadas da medula óssea é dependente do volume de treinamento físico aeróbio

“…Recent studies evidenced aerobic ET as responsible for promoting higher release and improving the bone-marrow derived EPC functional properties both in humans and animals, which contributes to the improvement of the endothelial function, angiogenesis and consequently, maintenance of cardiovascular homeostasis [13][14][15][16][17][18][19] . Although the ET effect on the EPC parameters has been evidenced, studies with alteration in the ET volume on the EPC and the capillarization have not been found yet.…”