Limits...
The combined effects of sidestream smoke extracts and glycated serum albumin on endothelial cells and platelets.

Rubenstein DA, Morton BE, Yin W - Cardiovasc Diabetol (2010)

Bottom Line: In general, the endothelial cell culture conditions were reduced in the presence of AGE and SHS.Nicotine, did not play a role in this reduction.This study also provides a new experimental technique to monitor platelet-endothelial cell interactions.

View Article: PubMed Central - HTML - PubMed

Affiliation: School of Mechanical and Aerospace Engineering, Oklahoma State University, Stillwater, USA. david.rubenstein@okstate.edu

ABSTRACT

Background: 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. 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.

Methods: Human 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.

Results: In 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.

Conclusions: Our 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.

Show MeSH

Related in: MedlinePlus

HUVEC viability (A) and density (B) as a function of combined media additives in the presence of platelets (pt). Data are the mean + SEM of 7 independent experiments. * differs from control (ANOVA, P < 0.05). + connected groups differ (ANOVA, P < 0.05)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2909174&req=5

Figure 4: HUVEC viability (A) and density (B) as a function of combined media additives in the presence of platelets (pt). Data are the mean + SEM of 7 independent experiments. * differs from control (ANOVA, P < 0.05). + connected groups differ (ANOVA, P < 0.05)

Mentions: In this study, our aim was to determine the combined effects of SHS and AGE on platelets and endothelial cells. To investigate this, we cultured endothelial cells in the presence of platelets and measured the endothelial cell culture response variables (cell viability and density) as well as the surface expression of GPIIb (CD41) on the platelet surface. In general, with any incubation that included SHS, the endothelial cell viability and cell density was significantly reduced as compared to the control samples (Figure 4). Interestingly, these parameters were slightly enhanced as compared to the endothelial cell incubation without platelets (Figure 1), suggesting that there is some interaction between platelets and endothelial cells which may act to delay cardiovascular disease progression. As before, nicotine did not mediate any of the changes seen here. Platelets followed a similar trend as endothelial cells (Figure 5), where the response measurement for platelets (GPIIb expression), was significantly enhanced after exposure to SHS, but this was generally attenuated as compared with the actions of SHS and AGE on platelets not in the presence of endothelial cells (Figures 3 vs. Figure 5). Combined, the endothelial cell and platelet data suggests that when incubated together, both the endothelial cell responses and the platelet responses are diminished as compared to the responses when the cells are not incubated together.


The combined effects of sidestream smoke extracts and glycated serum albumin on endothelial cells and platelets.

Rubenstein DA, Morton BE, Yin W - Cardiovasc Diabetol (2010)

HUVEC viability (A) and density (B) as a function of combined media additives in the presence of platelets (pt). Data are the mean + SEM of 7 independent experiments. * differs from control (ANOVA, P < 0.05). + connected groups differ (ANOVA, P < 0.05)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2909174&req=5

Figure 4: HUVEC viability (A) and density (B) as a function of combined media additives in the presence of platelets (pt). Data are the mean + SEM of 7 independent experiments. * differs from control (ANOVA, P < 0.05). + connected groups differ (ANOVA, P < 0.05)
Mentions: In this study, our aim was to determine the combined effects of SHS and AGE on platelets and endothelial cells. To investigate this, we cultured endothelial cells in the presence of platelets and measured the endothelial cell culture response variables (cell viability and density) as well as the surface expression of GPIIb (CD41) on the platelet surface. In general, with any incubation that included SHS, the endothelial cell viability and cell density was significantly reduced as compared to the control samples (Figure 4). Interestingly, these parameters were slightly enhanced as compared to the endothelial cell incubation without platelets (Figure 1), suggesting that there is some interaction between platelets and endothelial cells which may act to delay cardiovascular disease progression. As before, nicotine did not mediate any of the changes seen here. Platelets followed a similar trend as endothelial cells (Figure 5), where the response measurement for platelets (GPIIb expression), was significantly enhanced after exposure to SHS, but this was generally attenuated as compared with the actions of SHS and AGE on platelets not in the presence of endothelial cells (Figures 3 vs. Figure 5). Combined, the endothelial cell and platelet data suggests that when incubated together, both the endothelial cell responses and the platelet responses are diminished as compared to the responses when the cells are not incubated together.

Bottom Line: In general, the endothelial cell culture conditions were reduced in the presence of AGE and SHS.Nicotine, did not play a role in this reduction.This study also provides a new experimental technique to monitor platelet-endothelial cell interactions.

View Article: PubMed Central - HTML - PubMed

Affiliation: School of Mechanical and Aerospace Engineering, Oklahoma State University, Stillwater, USA. david.rubenstein@okstate.edu

ABSTRACT

Background: 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. 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.

Methods: Human 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.

Results: In 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.

Conclusions: Our 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.

Show MeSH
Related in: MedlinePlus