Novel Biomarkers for Coronary Restenosis Occurrence After Drug-Eluting Stent Implantation in Patients With Diabetes Having Stable Coronary Artery Disease

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The Impact of Hyperglycemia on VEGF Secretion in Retinal Endothelial Cells

AbstractBackground:Diabetic retinopathy is a serious sight-threatening complication which is manifested by excessive angiogenesis in diabetic patients.Aim:We hypothesize that cultured Rhesus monkey retinal endothelial cells (RhRECs) respond to high glucose with a change in cell proliferation and vascular endothelial growth factor (VEGF) secretion.Materials and methods:In our study, 20 000 cells per well were treated without glucose or with 5.5 mM, 18.5 mM and 30 mM glucose for 24 hours. Viable cells were counted using trypan blue dye exclusion method. VEGF concentrations were measured in cell media by ELISA method.Results:The number of viable cells incubated with 5.5 mM glucose increased significantly by 53.7% after 24 hours. In comparison, the number of viable cells decreased by 2.8% at 18.5 mM of glucose and by 20.4% at 30 mM of glucose after 24 hours of incubation. In contrast to this effect of glucose on the number of viable cells, a significant increase in VEGF levels (pg/mL) in the cell media with a glucose concentration of 0 mM compared to 5.5 mM of glucose was found. VEGF secretion in cell medium with 18.5 and 30 mM of glucose increased non-significantly in comparison with euglycemic levels.Conclusion:Our results show that viability of retinal endothelial cells and VEGF release are highly responsive to changes in glucose concentration. Such glucose-induced changes in retinal endothelial cells may negatively impact the integrity of the microvasculature in the diabetic retina leading to angiogenesis and microaneursym.</jats:p

H2S causes contraction and relaxation of major arteries of the rabbit

Objective: Cardiovascular disease (CVD) caused by atherosclerosis remains a worldwide burden. Hydrogen sulfide is a promising new therapeutic avenue for the treatment of CVD, however reports show exogenous H2S has both vasodilator and vasoconstrictor effects depending on organ examined, and in vitro studies in animal models which are not resistant to developing atherosclerosis are limited. We sought to determine if rabbit arteries constricted or dilated to hydrogen sulfide. Material and methods: The aorta, carotid, renal and iliac arteries were harvested from New Zealand White rabbits (n = 4) and subjected to a concentration response curve to the fast H2S releaser NaHS. In addition, a bolus dose of NaHS was used to determine if further dilation was achievable after maximum dilation to acetylcholine similar to nitric oxide donors. Further, NaHS was used to determine if H2S could impair homocysteine induced endothelial dysfunction. Results: Blood vessels relaxed poorly to NaHS and contracted at higher doses. A bolus dose of NaHS relaxed then contracted the aorta, however a bolus dose of NaHS after maximal relaxation to acetylcholine caused marked contraction. NaHS did not prevent homocysteine induced vascular dysfunction. Conclusion: NaHS at low doses caused minor relaxation of rabbit blood vessels, indicating a possible therapeutic benefit for low dose H2S in the cellular milieu