ABSTRACT
Objective To investigate the expressions of platelet activation-dependent granule membrane protein and platelet-derived growth factor receptor-αB, and the ultra-microstructure changes of platelets in patients with acute ST-segment elevation myocardial infarction(STEMI). Method The expressions of platelet activationdependent granule of glycoprotein (CD62P)and platelet derived growth factor receptor αβ subtype (PDGFR-αβ)of platelets in peripheral blood in 36 patients with acute ST-segment elevation myocardial infarction(STEMI) hospitalized and another 34 healthy subjects over the same period (control group) were investigated by flow cytometry and data were analyzed. The changes of ultra microstructure and activity of blood platelets in those patients and control group were observed under the scanning electron microscope. Results The expressions of CD62P and PDGFR-αβin patients with STEMI group before treatment were (3.65 ± 1.87) % and (0.43 ± 0.39) %, respectively, and those after treatment were (0.96 ± 0.79) % and (0.28 ± 0. 24) %, respectively, whereas those in control group were (0.67 ± 0.35) % and (0.27 ± 0.22) %, respectively, which were much lower in control than those in patients with STEMI before treatment (P ＜ 0.01 or P ＜ 0.05) respectively. There were statistically significant differences in the expressions of CD62P and PDGFR-αβ in patients group between pre-treatment and posttreatment (P ＜0.01 or P ＜0.05), respectively. Obvious ultra-microstructure changes of platelet surface in patients with STEMI group were observed. Conclusions Due to platelet activation in AMI, the expressions of CD62P can be used as effective indicators for monitoring coronary heart disease, and the PDGFR-αβ can be used as a reference indicator. The platelet surface ultra-microstructure changes during platelet activation in patients with AMI can be found by scanning electron microscopy.
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AIM: To investigate the effect of vasodilator-stimulated phosphoprotein (VASP) phosphorylation on the cell migration induced by platelet-derived growth factor BB (PDGF-BB), and to identify which phosphorylation site was more important among the three phosphorylation sites, namely Ser157,Ser239 and Thr278. METHODS: Two phosphorylation mutants of VASP, pcDNA3.1(+)/VASP-S157A and pcDNA3.1(+)/VASP-S239A, were constructed and respectively transfected into the cultured ECV304 cells by means of liposome. The stable expression cells were screened by using antibiotic G418. Protein expression of VASP was measured by Western blotting. The ECV304 cell migration was evaluated using Transwell chamber. RESULTS: Compared to control group, the cell migration was significantly inhibited in ECV304 transfected with VASP-S157A and VASP-S239A (P<0.05), although slight differences existed between VASP-S157A and VASP-S239A transfected cells (P>0.05). CONCLUSION: VASP mutation on the phosphorylation sites of Ser157 and Ser239 inhibits cell migration, and the phosphorylation sites of Ser157 and Ser239 both greatly affect the function of VASP.
ABSTRACT
AIM: To investigate the effects of sodium ferulate on cholesterol and triglyceride metabolism in atherosclerosis with hyperlipidemia.METHODS: The rabbit model of atherosclerosis was produced by feeding high lipid forages.RAW264.7 foam cell and HepG2 injured cell models were established by incubation with oxidized low density lipoprotein(ox-LDL).The atherosclerotic plaque area was measured,and serum lipids were detected.The cellular lipid accumulation was examined by oil red O staining.The cellular contents of total cholesterol and cholesterol ester were quantified by high performance liquid chromatography.The hepatic lipase(HL) mRNA expression was determined by RT-PCR.RESULTS:(1) Compared with hyperlipid group,the aorta atherosclerosis plaque area and the serum triglyceride level were significantly decreased in sodium ferulate-treated rabbits,but the serum cholesterol level showed little change.(2) Compared with ox-LDL group,the HL mRNA expression in HepG2 cells was enhanced significantly in sodium ferulate-treated group,but the cellular contents of total cholesterol and cholesterol ester in RAW264.7 foam cells showed little change.CONCLUSION: Sodium ferulate inhibits the formation of atherosclerotic plaque in high-cholesterol-fed rabbits aorta.This antiatherosclerotic function may reduce serum triglyceride level through enhancing the expression of HL mRNA without influencing serum cholesterol level and foam cell formation.