Han Wen-Qi, Chang Feng-Jun, Wang Qun-Rang, Pan Jun-Qiang
Cardiology. 2015;132(4):252-60. doi: 10.1159/000438782.
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.
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(O 2 – ) production. The origin of MPs was assessed by flow cytometry.
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 O 2 – generation in rat thoracic aortas. Endothelial-derived MPs and platelet-derived MPs made up nearly 75% of MPs.
Our data indicate that MPs from ACS patients negatively affect endothelial-dependent vasodilatation via Akt/eNOS-Hsp90 pathways.
内皮功能障碍参与急性冠脉综合征（ACS）的发生发展。其他疾病来源的血浆微粒（MPs）已被证明可引发凝血和内皮功能障碍。然而，ACS患者来源的MPs是否会损害血管舒张和内皮功能仍不清楚。
招募62例ACS患者和30例健康对照者进行MP分离。将大鼠胸主动脉与ACS患者或健康对照者来源的MPs共同孵育，以确定MPs对内皮依赖性血管舒张、Akt和内皮型一氧化氮合酶（eNOS）磷酸化、eNOS与热休克蛋白90（Hsp90）相互作用以及一氧化氮（NO）和超氧阴离子（O₂⁻）生成的影响。通过流式细胞术评估MPs的来源。
与健康对照者相比，ACS患者的MP浓度升高。它们与冠状动脉狭窄程度呈正相关。ACS患者来源的MPs损害内皮依赖性血管舒张，降低Akt和eNOS磷酸化水平，减少eNOS与Hsp90之间的相互作用，降低NO生成，但增加大鼠胸主动脉中O₂⁻的产生。内皮来源的MPs和血小板来源的MPs占MPs的近75%。
我们的数据表明，ACS患者来源的MPs通过Akt/eNOS-Hsp90途径对内皮依赖性血管舒张产生负面影响。
