The role of microparticles in oxidative stress and inflammation in patients with vascular intimal hyperplasia.

Abstract

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.