TY - JOUR
T1 - Short-term E-cigarette exposure increases the risk of thrombogenesis and enhances platelet function in mice
AU - Qasim, Hanan
AU - Karim, Zubair A.
AU - Silva-Espinoza, Juan C.
AU - Khasawneh, Fadi T.
AU - Rivera, José O.
AU - Ellis, Cameron C.
AU - Bauer, Stephanie L.
AU - Almeida, Igor C.
AU - Alshbool, Fatima Z.
N1 - Funding Information:
We are thankful to the Biomolecule Analysis Core Facility, Border Biomedical Research Center of the University of Texas at El Paso (BBRC/UTEP), supported by a grant (2G12MD007592) from the National Institute on Minority Health and Health Disparities (NIMHD), for the access to the liquid chromatography–mass spectrometry instrument used in this study. We are also grateful to our undergraduate students, Julien Esquivel and Dante Lozano, and our research assistant, Keziah R. Hernandez, for their help.
Funding Information:
This research was supported, in part, by startup funds provided by the School of Pharmacy, the University of Texas at El Paso (to Alshbool).
Publisher Copyright:
© 2018 The Authors.
PY - 2018/8/1
Y1 - 2018/8/1
N2 - Background-Cardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e-cigarettes are “safer/less harmful” than conventional cigarettes, their usage-among a variety of ages-has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e-cigarettes on the cardiovascular system, which is also the subject of significant debate. Methods and Results-We employed a passive e-Vape™ vapor inhalation system and developed an in vivo whole-body e-cigarette mouse exposure protocol that mimics real-life human exposure scenarios/conditions and investigated the effects of e-cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e-cigarette-exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air-exposed platelets. E-cigarette-exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e-cigarette-exposed mice exhibited a shortened thrombosis occlusion and bleeding times. Conclusions-Taken together, our data demonstrate for the first time that e-cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e-cigarette exposure should not be underestimated and warrant further investigation.
AB - Background-Cardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e-cigarettes are “safer/less harmful” than conventional cigarettes, their usage-among a variety of ages-has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e-cigarettes on the cardiovascular system, which is also the subject of significant debate. Methods and Results-We employed a passive e-Vape™ vapor inhalation system and developed an in vivo whole-body e-cigarette mouse exposure protocol that mimics real-life human exposure scenarios/conditions and investigated the effects of e-cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e-cigarette-exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air-exposed platelets. E-cigarette-exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e-cigarette-exposed mice exhibited a shortened thrombosis occlusion and bleeding times. Conclusions-Taken together, our data demonstrate for the first time that e-cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e-cigarette exposure should not be underestimated and warrant further investigation.
KW - Cardiovascular disease
KW - E-cigarettes
KW - E-vaping
KW - Electronic nicotine delivery systems
KW - Platelet
KW - Thrombosis
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U2 - 10.1161/JAHA.118.009264
DO - 10.1161/JAHA.118.009264
M3 - Article
C2 - 30021806
AN - SCOPUS:85051433473
SN - 2047-9980
VL - 7
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 15
M1 - e009264
ER -