Objectives: Endothelial dysfunction is involved in the development of the acute coronary syndrome (ACS). Plasma microparticles (MPs) from other diseases have been demonstrated to initiate coagulation and endothelial dysfunction. However, whether MPs from ACS patients impair vasodilatation and endothelial function remains unclear. Methods: Patients (n = 62) with ACS and healthy controls (n = 30) were recruited for MP isolation. Rat thoracic aortas were incubated with MPs from ACS patients or healthy controls to determine the effects of MPs on endothelial-dependent vasodilatation, the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), the interaction of eNOS with heat shock protein 90 (Hsp90), and nitric oxide (NO) and superoxide anion (O₂^-) production. The origin of MPs was assessed by flow cytometry. Results: MP concentrations were increased in patients with ACS compared with healthy controls. They were positively correlated with the degree of coronary artery stenosis. MPs from ACS patients impair endothelial-dependent vasodilatation, decrease both Akt and eNOS phosphorylation, decrease the interaction between eNOS and Hsp90, and decrease NO production but increase O₂^- generation in rat thoracic aortas. Endothelial-derived MPs and platelet-derived MPs made up nearly 75% of MPs. Conclusions: Our data indicate that MPs from ACS patients negatively affect endothelial-dependent vasodilatation via Akt/eNOS-Hsp90 pathways.

as a common factor of both type 2 diabetes mellitus (T2dM) and acute coronary syndrome (acS), circulating microparticles (MPs) may provide a link between these two diseases. The present study compared the content and function of MPs from patients with acS with or without T2dM. MPs from healthy subjects (n=20), patients with acS (n=24), patients with T2dM (n=20) and patients with combined acS and T2dM (n=24) were obtained. after incubating rat thoracic tissue with MPs, the effect of MPs on endothelial-dependent vasodilatation, expression of caveolin-1 and endothelial nitric oxide synthase (eNOS), phosphorylation of enoS at the S1177 and T495 sites and its association with heat shock protein 90 (Hsp90), and the generation of no and superoxide anion (o 2˙-) were determined. MP concentrations were higher in patients with T2dM and patients with acS with or without T2dM than in healthy subjects. Moreover, MPs from patients with T2dM or acS led to impairment in endothelial-dependent vasodilatation, decreased expression of no, as well as enoS and its phosphorylation at Ser1177 and association with Hsp90, but increased enoS phosphorylation at T495, caveolin-1 expression and o 2˙-generation. These effects were strengthened by MPs from patients with acS combined with T2dM. T2dM not only increased MP content but also resulted in greater vascular impairment effects in acS. These results may provide novel insight into the treatment of patients with acS and T2dM.

Objective. High-density lipoprotein (HDL) was found vasoprotective, but numbers of patients with acute myocardial infarction (AMI) have normal or even high levels of pathological HDL (pHDL). So, we investigate the mechanism of pHDL in AMI patients on angiogenesis. Methods. HDL with normal levels from healthy subjects (nHDL, control group, n = 20 ) and patients with AMI (pHDL, experimental groups, n = 30 ) were obtained by super high speed centrifugation. Then, effects of HDL on proliferation, migration, angiogenesis, and expression of ERK1/2 and its phosphorylation in human umbilical vein endothelial cells (HUVEC) with or without PD98059 (inhibitor of ERK1/2) preincubation were detected. Results. Compared with the control group (nHDL), HDL from the experimental group (pHDL) significantly inhibited the phosphorylation of ERK1/2, proliferation, migration, and angiogenesis of HUVEC ( P < 0.05 ), while these effects of HDL could substantially be blocked by preincubation of PD98059 ( P < 0.05 ). Conclusion. HDL in AMI patients affects angiogenesis by inhibiting ERK1/2 activation free from HDL levels.