Abstract
BackgroundThe purpose of this study was to test the hypothesis that sidestream tobacco smoke extracts would inhibit the culture of endothelial cells and enhance platelet aggregation under diabetic vascular conditions. Sidestream tobacco smoke and advanced glycation end products are known cardiovascular risk factors and we aimed to determine the combined interaction between these two risk factors to promote cardiovascular diseases associated with diabetes.MethodsHuman umbilical vein endothelial cells were cultured in the presence of sidestream tobacco smoke extracts (SHS) or nicotine and glycated albumin (AGE) or non-glycated albumin. After 3 days, endothelial cell viability and density were investigated. Platelets were also incubated with these compounds for up to 6 hours. Platelet aggregation and the surface expression of CD41 and CD62P were examined. In some experiments, platelets were added to the endothelial cell culture to determine if an interaction between platelets and endothelial cells occurs that can alter the responses to SHS or AGE.ResultsIn general, the endothelial cell culture conditions were reduced in the presence of AGE and SHS. Nicotine, did not play a role in this reduction. Platelet aggregation proceeded faster in the presence of AGE and SHS. Interestingly, with the combined culture of endothelial cells and platelets, the endothelial cell culture conditions were improved and the platelet functional changes were diminished in the presence of SHS and AGE, as compared with the individual incubations.ConclusionsOur data suggests that diabetics that are exposed to SHS may have a higher likelihood for cardiovascular disease development through a diminished endothelial cell viability and an increased platelet activity, which are partially mediated by CD41 and not CD62P. This study provides support for an increased cardiovascular risk for diabetic patients that are exposed to SHS. This study also provides a new experimental technique to monitor platelet-endothelial cell interactions.
Highlights
The purpose of this study was to test the hypothesis that sidestream tobacco smoke extracts would inhibit the culture of endothelial cells and enhance platelet aggregation under diabetic vascular conditions
We investigated the changes in platelet activation, aggregation and cell surface marker expression in response to the combined exposure to advanced glycation end products and sidestream tobacco smoke extracts or nicotine
Endothelial Cell Response To test the endothelial cell response towards the combined effects of secondhand smoke tobacco smoke extracts (SHS) and glycated serum albumin, first we investigated the individual responses to various additives to the cell culture media
Summary
The purpose of this study was to test the hypothesis that sidestream tobacco smoke extracts would inhibit the culture of endothelial cells and enhance platelet aggregation under diabetic vascular conditions. The risk for cardiovascular disease formation is highly correlated to the exposure to environmental tobacco smoke, as either mainstream (i.e. the smoker) or sidestream (i.e. secondhand from the smoldering cigarette), and to the occurrence of diabetes. While the effects of cigarette smoke are multifactorial, it has been previously shown that secondhand smoke (SHS) can enhance tumor formation[4], vascular permeability[5] and inflammatory responses[6], which can all lead to cardiovascular disease formation. Nicotine, which is the primary psychoactive component of cigarettes, can enhance the surface expression of some endothelial cell inflammatory mediators[7] and can accelerate some cardiovascular disease formation[8]. Platelet activation and aggregation are enhanced after exposure to secondhand smoke[9,10], whereas nicotine strongly inhibits platelet activation[10,11]
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