Low Levels of Endothelial Progenitor Cells and Their Association with Systemic Inflammation and Monocyte Activation in Older HIV-Infected Men
Year: 2017
Type: article
Study design: Observational Study
Abstract: Endothelial progenitor cells (EPCs) repair damaged vascular endothelium, and low circulating EPC levels have been associated with cardiovascular disease (CVD). CD34 + /KDR + EPCs are commonly reported in the literature and CD34 + /CD133 + /KDR + EPCs are rare in circulation but highly specific for endothelial lineage. HIV-infected (HIV+) adults have chronic inflammation and increased CVD risk, but the relationship between CVD, vascular inflammation, and EPCs in HIV remains unclear. In a pilot study, EPCs were measured in 57 HIV+ men [≥50 years old, HIV-1 RNA <50 copies/ml on antiretroviral therapy (ART)] by real-time flow cytometry using cellular immaturity (CD34 and/or CD133) and endothelial commitment (KDR) markers. Fasting inflammatory biomarker levels were measured by ELISA. Median age was 57 years; CD4 + T lymphocyte count was 570 cells/mm 3 . Prevalent CVD risk factors included 16% diabetes, 28% hypertension, 53% dyslipidemia, and 33% smoking. Median (interquartile range) EPC values were CD34 + /KDR + 0.1 (0.0–0.9) cells/10 5 peripheral blood mononuclear cells (PBMCs) and CD34 + /CD133 + /KDR + 0.1 (0.0–0.9) cells/10 5 PBMCs. We observed a high prevalence of undetectable CD34 + /KDR + (40%) and CD34 + /CD133 + /KDR + EPCs (44%). Men with undetectable EPCs were more likely to have ≥2 CVD risk factors, lower interleukin-6 (IL-6), and higher sCD163 levels. In these older HIV+ men on suppressive ART, CD34 + /KDR + and CD34 + /CD133 + /KDR + EPC levels were low and often undetectable. Undetectable EPC levels were associated with greater CVD risk factor burden, lower IL-6 (consistent with decreased EPC production stimulus), and higher sCD163 (consistent with monocyte activation and prior CVD associations) levels, suggesting a potential relationship between EPCs and atherosclerotic burden in this population.
Institutions: Inserm, Sorbonne Université, Assistance Publique – Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Institut Pierre Louis d‘Épidémiologie et de Santé Publique, Université Pierre-et-Marie-Curie, University of California, Los Angeles, University of California System, The University of Texas Health Science Center at Houston
Language: English
Subfield: Emergency Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: Oxidized HDL in the intersection of HIV, immune activation and atherosclerosis, Targeting early instigators of vascular inflammation to prevent and/or delay vascular aging in chronic treated HIV, Inflammation, Fibrosis and End-Organ Disease in HIV-Infected Adults, Elucidating the impact of molecular signatures of immune senescence on aging in chronic treated HIV, UCLA Center for AIDS Research (CFAR), UCLA Older Americans Independence Center, G9000014846, G9000249658
OpenAlex ID: W2983800485