Circulating CD34 + cell subsets in patients with coronary endothelial dysfunction

• Published in: Nature clinical practice cardiovascular medicine Vol. 5; no. 8; pp. 489 - 496
• Main Authors: Simari, Robert D, Boilson, Barry A, Kiernan, Thomas J, Harbuzariu, Adriana, Nelson, Rebecca E, Lerman, Amir
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 01.08.2008
• Subjects: Adult; Antigens, CD34 - blood; Coronary Artery Disease - blood; Coronary Artery Disease - immunology; Endothelium, Vascular - physiopathology; Female; Flow Cytometry; Gene Expression; Humans; Male; Middle Aged
• ISSN: 1743-4297; 1759-5002; 1743-4300; 1759-5010
• DOI: 10.1038/ncpcardio1277

Endothelial dysfunction is an early manifestation of atherosclerotic disease. Circulating cells that express CD34, including endothelial and hematopoietic progenitor cells, might play a part in the development and progression of atherosclerosis. The aim of this study was to evaluate the association between coronary endothelial dysfunction and concentrations of circulating CD34+ cell subsets. Intracoronary acetylcholine challenge was used to test for coronary endothelial dysfunction in 57 consecutive patients scheduled to undergo diagnostic coronary angiography and with no signs of substantial obstructive lesions. Mononuclear cells were extracted from whole blood samples taken from all patients, analyzed by flow cytometry for CD14, CD34, CD133, CD45, and vascular endothelial growth factor receptor 2 (VEGFR2), and cultured for functional analysis. Compared with patients with normal coronary endothelial function, in those with coronary endothelial dysfunction, the number of circulating CD34+/CD45(dim)/VEGFR2- cells, CD34+/CD45(dim)/CD133+/VEGFR2- cells and colony-forming units were reduced. Concentrations of CD34+/CD45-/VEGFR2+ cells did not differ between groups. Regulation of CD34+ cell subsets seems to differ between patients with coronary endothelial dysfunction and those with normal coronary endothelial function. Changes in specific circulating progenitor cell subsets might, therefore, be an early manifestation of atherosclerosis.