+ Site Statistics
References:
52,572,879
Abstracts:
28,705,754
PMIDs:
27,750,366
DOIs:
25,464,004
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Brief secondhand smoke exposure depresses endothelial progenitor cells activity and endothelial function: sustained vascular injury and blunted nitric oxide production



Brief secondhand smoke exposure depresses endothelial progenitor cells activity and endothelial function: sustained vascular injury and blunted nitric oxide production



Journal of the American College of Cardiology 51(18): 1760-1771



This study sought to analyze the effects of acute secondhand smoke (SHS) exposure on the number and function of endothelial progenitor cells (EPCs) over 24 h. Secondhand smoke increases the risk of vascular disease and is a major public health concern, but the mechanism(s) of action are not fully understood. Healthy nonsmokers (age SEM 30.3 +/- 1.3 years, n = 10) were exposed to 30 min of SHS yielding cotinine levels commonly observed in passive smokers and to smokefree air on 2 separate days. Measurements were taken before exposure (baseline), immediately after (0 h), and at 1 h, 2.5 h, and 24 h after. The EPCs (CD133(+)/KDR(+), CD34(+)/KDR(+)) and endothelial microparticles (EMPs: CD31(+)/CD41(-), CD144(+), CD62e(+)) were determined in blood using flow cytometry. The EPC chemotaxis toward vascular endothelial growth factor was measured. Endothelial function was assessed as flow-mediated dilation (FMD) using ultrasound. Secondhand smoke exposure increased EPCs and plasma vascular endothelial growth factor and completely abolished EPC chemotaxis during 24 h after exposure. Secondhand smoke increased EMPs and decreased FMD. Although FMD returned to baseline at 2.5 h, EMPs and vascular endothelial growth factor levels remained elevated at 24 h, suggesting endothelial activation and injury with functional impairment of the vascular endothelium. Exposure to smokefree air had no effect. Incubation of EPCs from nonexposed subjects with plasma isolated from SHS-exposed subjects in vitro decreased chemotaxis by blockade of vascular endothelial growth factor-stimulated nitric oxide production. Brief exposure to real-world levels of SHS leads to sustained vascular injury characterized by mobilization of dysfunctional EPCs with blocked nitric oxide production. Our results suggest that SHS not only affects the vascular endothelium, but also the function of EPCs.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 051868175

Download citation: RISBibTeXText

PMID: 18452782

DOI: 10.1016/j.jacc.2008.01.040


Related references

One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function. Journal of the American Heart Association 5(8), 2018

Endothelial nitric oxide synthase protein distribution and nitric oxide production in endothelial cells along the coronary vascular tree. Microvascular Research 122: 34-40, 2018

Involvement of endothelial nitric oxide synthase pathway in IGF‑1 protects endothelial progenitor cells against injury from oxidized LDLs. Molecular Medicine Reports 2018, 2018

Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II. Molecular Medicine Reports 16(5): 6255-6261, 2017

Hydrogen sulfide improves vascular repair by promoting endothelial nitric oxide synthase-dependent mobilization of endothelial progenitor cells. Journal of Hypertension 2018, 2018

Attenuated endothelial function is associated with decreased endothelial progenitor cells and nitric oxide in premenopausal diabetic women. Molecular Medicine Reports 18(5): 4666-4674, 2018

Phosphorylation of tyrosine 801 of vascular endothelial growth factor receptor-2 is necessary for Akt-dependent endothelial nitric-oxide synthase activation and nitric oxide release from endothelial cells. Journal of Biological Chemistry 282(14): 10660-9, 2007

Short-term exposure of bovine aortic endothelial cells to H2O2 results in a sustained increase in endothelial nitric oxide synthase expression. FASEB Journal 13(4 PART 1): A368, March 12, 1999

Sustained pulsatile flow regulates endothelial nitric oxide synthase and cyclooxygenase expression in co-cultured vascular endothelial and smooth muscle cells. Journal of Molecular and Cellular Cardiology 31(3): 619-629, 1999

Autocrine release of vascular endothelial growth factor-A and nitric oxide plays an important role in the development and proliferation of human endothelial progenitor cells. Circulation 100(18 SUPPL ): I 406, Nov 2, 1999

Vascular endothelial growth factor acts through novel, pregnancy-enhanced receptor signalling pathways to stimulate endothelial nitric oxide synthase activity in uterine artery endothelial cells. Biochemical Journal 417(2): 501-511, 2008

GW28-e0957 Smoke-induced decreased nitric oxide production contributes to upregulation of circulating endothelial progenitor cells and deterioration in arterial elasticity in healthy men. Journal of the American College of Cardiology 70(16): C35-C36, 2017

Estrogen-mediated, endothelial nitric oxide synthase-dependent mobilization of bone marrow-derived endothelial progenitor cells contributes to reendothelialization after arterial injury. Circulation 108(25): 3115-3121, 2003

Cigarette Smoke Extract Changes Expression of Endothelial Nitric Oxide Synthase (eNOS) and p16(INK4a) and is Related to Endothelial Progenitor Cell Dysfunction. Medical Science Monitor 23: 3224-3231, 2018

Pregnancy enhances sustained Ca2+ bursts and endothelial nitric oxide synthase activation in ovine uterine artery endothelial cells through increased connexin 43 function. Biology of Reproduction 82(1): 66-75, 2010