Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function

• Published in: Journal of the American College of Cardiology Vol. 51; no. 18; pp. 1760 - 1771
• Main Authors: Heiss, Christian, MD, Dr Med, Amabile, Nicolas, MD, Lee, Andrew C., MD, Real, Wendy May, BS, Schick, Suzaynn F., PhD, Lao, David, MD, Wong, Maelene L., BS, Jahn, Sarah, MB, Angeli, Franca S., MD, Minasi, Petros, BA, Springer, Matthew L., PhD, Hammond, S. Katharine, PhD, Glantz, Stanton A., PhD, FACC, Grossman, William, MD, FACC, Balmes, John R., MD, Yeghiazarians, Yerem, MD, FACC
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 06.05.2008
• Subjects: Cardiovascular; Internal Medicine; NO; nitric oxide; diaminofluorescein; VEGF; DAF; EMP; endothelial progenitor cell; phycoerythrin; UEA; BSA; L G-monomethyl-arginine; bromodeoxyuridine; PE; vascular endothelial growth factor; endothelial microparticle; EPC; flow-mediated dilation; L-NMMA; FMD; secondhand smoke; BrdU; bovine serum albumin; Ulex europeus agglutinin; SHS
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2008.01.040

Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function: Sustained Vascular Injury and Blunted Nitric Oxide Production Christian Heiss, Nicolas Amabile, Andrew C. Lee, Wendy May Real, Suzaynn F. Schick, David Lao, Maelene L. Wong, Sarah Jahn, Franca S. Angeli, Petros Minasi, Matthew L. Springer, S. Katharine Hammond, Stanton A. Glantz, William Grossman, John R. Balmes, Yerem Yeghiazarians Secondhand smoke (SHS) increases the risk of vascular disease and is a major public health concern, but the mechanism(s) of action are not fully understood. We studied the effects of acute SHS exposure on the number and function of endothelial progenitor cells, plasma vascular endothelial growth factor, circulating endothelial microparticles, and flow-mediated vasodilation at serial time points until 24 h after exposure. Brief exposure to a real-world level of SHS not only causes acute vascular injury as indicated by endothelial dysfunction and microparticle generation, but also leads to sustained changes of the vascular repair system with a mobilization of dysfunctional endothelial progenitor cells.