Wang Xu-Lan, Han Wen-Qi, Yang Kun, Chang Feng-Jun, Zhang Wei, Li Zhe, Yang Yu-Juan
Faculty of medicine, Xian'yang Vocational and Technical College, P.R. China.
Department of Cardiology, Shaanxi Provincial People's Hospital and The Third Affiliated Hospital of Xi'an Jiaotong University, P.R. China.
J Int Med Res. 2025 Aug;53(8):3000605251364781. doi: 10.1177/03000605251364781. Epub 2025 Aug 12.
ObjectivesIntimal hyperplasia, which is mainly caused by vascular damage during percutaneous coronary intervention, affects the prognosis of patients who undergo percutaneous coronary intervention. However, it remains unclear whether circulating microparticles, which are also affected by percutaneous coronary intervention, participate in intimal hyperplasia.MethodsIn this applied basic research (also identified as a cross-sectional study), microparticles were obtained from healthy participants (n = 20), patients with serious intimal hyperplasia (n = 33), and patients with mild intimal hyperplasia (n = 33) 1 year after percutaneous coronary intervention. After origins testing, the effects of microparticles on the proliferation and migration (crucial processes in intimal hyperplasia) of human coronary artery smooth muscle cells were determined. The expression levels of extracellular signal-related kinase (ERK), p38 mitogen-activated protein kinase (P38), and c-Jun N-terminal kinase (JNK) as well as the production of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule 1 (markers related to oxidative stress, inflammation, and cell differentiation signaling pathways) were also evaluated.ResultsAlthough the microparticle concentration was higher in patients with mild and serious intimal hyperplasia than in healthy participants, there were no differences in the microparticle concentration between patients with mild and serious intimal hyperplasia. Flow cytometry revealed that the concentration of both endothelial-derived microparticles and platelet-derived microparticles increased in mild and serious intimal hyperplasia. Microparticles derived from patients with mild intimal hyperplasia stimulated the proliferation and migration of human coronary artery smooth muscle cells (partially blocked by PD98059); increased the phosphorylation of ERK and P38, but not JNK; and enhanced the production of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule 1 (blocked by SB20358). All these effects were more pronounced in patients with serious intimal hyperplasia.ConclusionsThe effects of microparticles in patients with intimal hyperplasia may reveal a therapeutic target for intimal hyperplasia.
目的
内膜增生主要由经皮冠状动脉介入治疗期间的血管损伤引起，影响接受经皮冠状动脉介入治疗患者的预后。然而，同样受经皮冠状动脉介入治疗影响的循环微粒是否参与内膜增生仍不清楚。
方法
在这项应用基础研究（也被确定为横断面研究）中，在经皮冠状动脉介入治疗1年后，从健康参与者（n = 20）、严重内膜增生患者（n = 33）和轻度内膜增生患者（n = 33）中获取微粒。在进行来源检测后，确定微粒对人冠状动脉平滑肌细胞增殖和迁移（内膜增生的关键过程）的影响。还评估了细胞外信号调节激酶（ERK）、p38丝裂原活化蛋白激酶（P38）和c-Jun氨基末端激酶（JNK）的表达水平，以及细胞间黏附分子-1和血管细胞黏附分子1（与氧化应激、炎症和细胞分化信号通路相关的标志物）的产生。
结果
尽管轻度和严重内膜增生患者的微粒浓度高于健康参与者，但轻度和严重内膜增生患者之间的微粒浓度没有差异。流式细胞术显示，轻度和严重内膜增生患者中内皮源性微粒和血小板源性微粒的浓度均增加。轻度内膜增生患者来源的微粒刺激人冠状动脉平滑肌细胞的增殖和迁移（部分被PD98059阻断）；增加ERK和P38的磷酸化，但不增加JNK的磷酸化；并增强细胞间黏附分子-1和血管细胞黏附分子1的产生（被SB20358阻断）。所有这些作用在严重内膜增生患者中更为明显。
结论
内膜增生患者中微粒的作用可能揭示了内膜增生的治疗靶点。
