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Cigarette Smoking-Associated Alterations in Serotonin/Adrenalin Signaling Pathways of Platelets
Curtis Lee Lowery1,2, Clay Elliott1,2, Anthonya Cooper1,2
1University of Arkansas for Medical Sciences, Little Rock, AR.
Journal of the American Heart Association
|May 20, 2017
Summary
Cigarette smoking significantly increases platelet aggregation and alters platelet surface proteins and glycans by elevating serotonin (5-HT) and catecholamine levels. This leads to hyperactive platelets, increasing cardiovascular disease risk.
Area of Science:
- Cardiovascular Biology
- Platelet Physiology
- Molecular Medicine
Background:
- Cigarette smoking is a major risk factor for cardiovascular diseases.
- Smoking acutely activates the sympathetic nervous system, increasing blood serotonin (5-HT) and catecholamine levels.
- The impact of these elevated levels on platelet biology and thrombosis risk requires further investigation.
Purpose of the Study:
- To investigate how cigarette smoking-induced elevations in plasma serotonin (5-HT) and catecholamine affect platelet biology.
- To explore the remodeling of platelet surface proteins and glycans in smokers.
Main Methods:
- Blood samples from smokers and nonsmokers were analyzed 15 minutes post-smoking.
- Platelet aggregation, plasma 5-HT/catecholamine concentrations, platelet membrane proteins, and platelet surface glycans were quantified.
- Liquid chromatography-tandem mass spectrometry and MALDI-MS were employed for molecular analysis.
Main Results:
- Smoking increased plasma 5-HT/catecholamine levels and platelet aggregation twofold.
- Smokers' platelet membranes showed elevated levels of GTPase-activating proteins and actin cytoskeletal proteins.
- Glycan analysis revealed distinct structural differences on smokers' platelet surfaces, which were modulated by blocking 5-HT/catecholamine receptors.
Conclusions:
- Smoking-induced 5-HT/catecholamine signaling accelerates platelet trafficking, remodeling surface proteins and glycans, leading to hyperactive platelets.
- Smokers' platelets exhibit increased intracellular calcium and transglutaminase activity.
- These findings link smoking, 5-HT/catecholamine signaling, and downstream pathways to elevated platelet activation in smokers, suggesting a mechanism for increased thrombosis risk.
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