title: Human aging and CD31+ T-cell number, migration, apoptotic susceptibility, and telomere length.
abstract: CD31(+) T cells, or so-called "angiogenic T cells," have been shown to demonstrate vasculoprotective and neovasculogenic qualities. The influence of age on CD31(+) T-cell number and function is unclear. We tested the hypothesis that circulating CD31(+) T-cell number and migratory capacity are reduced, apoptotic susceptibility is heightened, and telomere length is shortened with advancing age in adult humans. Thirty-six healthy, sedentary men were studied: 12 young (25 ± 1 yr), 12 middle aged (46 ± 1 yr), and 12 older (64 ± 2 yr). CD31(+) T cells were isolated from peripheral blood samples by magnetic-activated cell sorting. The number of circulating CD31(+) T cells (fluorescence-activated cell sorting analysis) was lower (P < 0.01) in older (24% of CD3(+) cells) compared with middle-aged (38% of CD3(+) cells) and young (40% of CD3(+) cells) men. Migration (Boyden chamber) to both VEGF and stromal cell-derived factor-1α was markedly blunted (P < 0.05) in cells harvested from middle-aged [306.1 ± 45 and 305.6 ± 46 arbitrary units (AU), respectively] and older (231 ± 65 and 235 ± 62 AU, respectively) compared with young (525 ± 60 and 570 ± 62 AU, respectively) men. CD31(+) T cells from middle-aged and older men demonstrated greater apoptotic susceptibility, as staurosporine-stimulated intracellular caspase-3 activation was ∼ 40% higher (P < 0.05) than young. There was a progressive age-related decline in CD31(+) T-cell telomere length (young: 10,706 ± 220 bp; middle-aged: 10,179 ± 251 bp; and older: 9,324 ± 192 bp). Numerical and functional impairments in this unique T-cell subpopulation may contribute to diminished angiogenic potential and greater cardiovascular risk with advancing age.
authors.affiliation: Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO 8030, USA.
authors.forename: Erich J
authors.initials: EJ
authors.lastname: Kushner
authors.forename: Brian R
authors.initials: BR
authors.lastname: Weil
authors.forename: Owen J
authors.initials: OJ
authors.lastname: MacEneaney
authors.forename: Richard G
authors.initials: RG
authors.lastname: Morgan
authors.forename: Michael L
authors.initials: ML
authors.lastname: Mestek
authors.forename: Gary P
authors.initials: GP
authors.lastname: Van Guilder
authors.forename: Kyle J
authors.initials: KJ
authors.lastname: Diehl
authors.forename: Brian L
authors.initials: BL
authors.lastname: Stauffer
authors.forename: Christopher A
authors.initials: CA
authors.lastname: DeSouza
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D000375:Aging / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D017209:Apoptosis / Q000235:genetics; D002318:Cardiovascular Diseases / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D002469:Cell Separation / Q000379:methods; D054377:Chemokine CXCL12 / Q000378:metabolism; D002633:Chemotaxis; D045304:Cytochromes c / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis*; D012307:Risk Factors; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D055815:Young Adult
chemical_list: D054377:Chemokine CXCL12; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D045304:Cytochromes c; D019098:Telomerase; C505407:CASP3 protein, human; D053148:Caspase 3