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.

Objectives: Intimal 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. Methods: In 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. Results: Although 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. Conclusions: The effects of microparticles in patients with intimal hyperplasia may reveal a therapeutic target for intimal hyperplasia.

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, ) and patients with AMI (pHDL, experimental groups, ) 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 ( ), while these effects of HDL could substantially be blocked by preincubation of PD98059 ( ). Conclusion. HDL in AMI patients affects angiogenesis by inhibiting ERK1/2 activation free from HDL levels.

Objective. We demonstrated that circulating microparticles (MPs) are increased in patients with coronary heart disease (both chronic coronary syndrome (CCS) and acute coronary syndrome). Whether thrombolysis affects MPs in patients with ST-segment elevation myocardial infarction (STEMI) with or without percutaneous coronary intervention (PCI) is unknown. Methods. This study was divided into three groups: STEMI patients with thrombolysis ( ) were group T, patients with chronic coronary syndrome ( ) were group CCS, and healthy volunteers ( ) were the control group. Fasting venous blood was extracted from patients in the CCS and control groups, and venous blood was extracted from patients in the T group before (pre-T) and 2 hours after (post-T) thrombolysis. MPs from each group were obtained by centrifugation. After determining the concentration, the effects of MPs on endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in rat myocardial tissue in vitro were detected by immunohistochemistry and western blotting. Changes in nitric oxide (NO) and oxygen free radicals (O₂^•–) were also detected. The effect of MPs on vasodilation in isolated rat thoracic aortae was detected. Results. Compared with that in the control group ( mg/ml), the concentration of MPs was increased in patients with CCS ( mg/ml) and in STEMI patients before thrombolysis ( mg/ml). However, thrombolysis did not further increase MP levels (post-T, mg/ml) compared with those in STEMI patients before thrombolysis. Compared with those in the control group, MPs in both CCS and STEMI patients before thrombolysis inhibited the expression of eNOS (both immunohistochemistry and western blot analysis of phosphorylation at Ser1177), NO production in the isolated myocardium and vasodilation in vitro and stimulated the expression of iNOS (immunohistochemistry and western blot analysis of phosphorylation at Thr495), and the generation of O₂^•– in the isolated myocardium. The effects of MPs were further enhanced by MPs from STEMI patients 2 hours after thrombolysis. Conclusion. Changes in MP function after thrombolysis may be one of the mechanisms leading to ischemia–reperfusion after thrombolysis.

Atherosclerosis is a severe cardiovascular disease characterized by narrowing of the lumen, plaque formation, and blood flow turbulence as a result of cholesterol and lipid accumulation in the inner lining of arteries. Bishkhapra (Trianthema portulacastrum Linn.) is a well-known common weed belonging to the family Aizoaceae. Several bioactive compounds have been isolated from this weed and widely used against several diseases. The present study evaluated the protective and therapeutic efficacies of T. portulacastrum against atherosclerosis in a rat model. The animals were divided into the sham, control (diabetes- + atherosclerosis-inducing diet), 100 mg/kg T. portulacastrum treatment, 200 mg/kg T. portulacastrum treatment, and positive control groups. Blood glucose, cholesterol, triglyceride, and other lipid parameters, as well as the expression of G-protein-coupled receptor 124 (GPR124), were measured. Glucose, cholesterol, and triglycerides were significantly reduced to near normal levels. The serum levels of fibrinogen, sVCAM-1, and oxidized low density lipoproteins were substantially increased in control rats. Treatment with the T. portulacastrum extract reversed these levels to near normal levels. The mRNA expression of GPR124 was increased by 150% in the control group. However, treatment with T. portulacastrum extract decreased the mRNA expression up to 40% compared with the control group. Rats treated with 100 and 200 mg/kg T. portulacastrum extract showed a decrease in GPR124 protein expression by 9.5% and 33.3%, respectively. Taken together, the results suggest that an extract of T. portulacastrum is effective against atherosclerosis in streptozotocin-induced diabetic rats.