Platelet activation, adhesion, inflammation, and aggregation potential are altered in the presence of electronic cigarette extracts of variable nicotine concentrations.
Tobacco smoke extracts prepared from both mainstream and sidestream smoking have been associated with heightened platelet activation, aggregation, adhesion, and inflammation. Conversely, it has been shown that pure nicotine inhibits similar platelet functions. In this work, we 1) evaluated the effects of e-cigarette extracts on platelet activities and 2) elucidated the differences between the nicotine-dependent and non-nicotine dependent (e.g. fine particulate matter or toxic compounds) effects of tobacco and e-cigarette products on platelet activities. To accomplish these goals, platelets from healthy volunteers (n = 50) were exposed to tobacco smoke extracts, e-cigarette vapor extracts, and pure nicotine and changes in platelet activation, adhesion, aggregation, and inflammation were evaluated, using optical aggregation, flow cytometry, and ELISA methods. Interestingly, the exposure of platelets to e-vapor extracts induced a significant up-regulation in the expression of the pro-inflammatory gC1qR and cC1qR and induced a marked increase in the deposition of C3b as compared with traditional tobacco smoke extracts. Similarly, platelet activation, as measured by a prothrombinase based assay, and platelet aggregation were also significantly enhanced after exposure to e-vapor extracts. Finally, platelet adhesion potential toward fibrinogen, von Willebrand factor, and other platelets was also enhanced after exposure to e-cigarette vapor extracts. In the presence of pure nicotine, platelet functions were observed to be inhibited, which further suggests that other constituents of tobacco smoke and electronic vapor can antagonize platelet functions, however, the presence of nicotine in extracts somewhat perpetuated the platelet functional changes in a dose-dependent manner.
a Department of Biomedical Engineering , Stony Brook University , Stony Brook , NY , USA.
Sarah
S
Hom
a Department of Biomedical Engineering , Stony Brook University , Stony Brook , NY , USA.
Li
L
Chen
a Department of Biomedical Engineering , Stony Brook University , Stony Brook , NY , USA.
Tony
T
Wang
b School of Medicine, Department of Medicine , Stony Brook University , Stony Brook , NY , USA.
Berhane
B
Ghebrehiwet
a Department of Biomedical Engineering , Stony Brook University , Stony Brook , NY , USA.
Wei
W
Yin
a Department of Biomedical Engineering , Stony Brook University , Stony Brook , NY , USA.
David A
DA
Rubenstein
D001792:Blood Platelets / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D066300:Electronic Nicotine Delivery Systems; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D009538:Nicotine / Q000494:pharmacology*; D015539:Platelet Activation / Q000187:drug effects*; D010973:Platelet Adhesiveness / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects*; D010979:Platelet Function Tests; D011485:Protein Binding; D011951:Receptors, Complement / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects
D008562:Membrane Glycoproteins; D011951:Receptors, Complement; C032402:complement 1q receptor; D009538:Nicotine; D003165:Complement System Proteins
Cardiovascular diseases; cardiovascular risk factors; coagulation; electronic cigarettes; platelets