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Exposure to E‐Vapor Extracts Alters Platelet Aggregation, Adhesion and Activation
Author(s) -
Chen Li,
Wang Tony,
Yin Wei,
Rubenstein David
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.631.6
Subject(s) - platelet , chemistry , platelet activation , coagulation , oxidative stress , nicotine , tobacco smoke , biophysics , biochemistry , immunology , medicine , biology , polymer chemistry
Cardiovascular diseases remain to be the leading cause of death in the Western world. Tobacco smoke is a well‐known instigator of cardiovascular diseases, primarily through the delivery of fine particulate matter and oxidative stressors. The effects of e‐cigarettes, a relatively new source of both fine particulate matter and oxidative stressors, on cardiovascular health has not been investigated thoroughly. Here, we aimed to elucidate if the exposure to physiologically relevant levels of e‐vapor can alter platelet functions. To accomplish this aim, we exposed platelets to e‐vapor extracts and quantified platelet aggregation, expression of adhesion, activation and aggregation markers and participation in coagulation based reactions. Platelet aggregation was enhanced after exposure to e‐vapor extracts and for the e‐juice formulations with the highest concentration of nicotine, this enhancement mirrored the effects of mainstream and sidestream tobacco smoke extracts. Altered platelet aggregation was partially induced by an up‐regulation of CD42b. Adhesion potential of platelets was also enhanced via an up‐regulation of CD41a and CD62P, respectively. Each of these adhesion enhancements was e‐juice nicotine concentration and exposure duration dependent. After exposure to e‐vapor, platelets were more likely to participate in coagulation based reactions, suggesting an enhancement of the coagulation cascade. Enhanced platelet activation was at least partially mediated by an increased expression of phosphatidylserine and a release of platelet a‐granules. These enhancements were both time and dose dependent. Thus, our data illustrates preliminary evidence that e‐vapor exposure may alter platelet functions associated with cardiovascular disease progression.