Abstract:The features of atherothrombotic diseases are the rupture of atherosclerotic plaques and thrombosis.Platelet activation and aggregation play a pivotal role in the pathogenesis and clinical manifestation.Similar to neuronal and immunological synapse,synaptic structure is also formed between platelets during thrombus formation.The microenvironment of platelet synapse facilitates signal transduction that has been accepted as contact-dependent events due to their occurrence after platelet contact begins,which is believed to play a role in the thrombus formation and stability.Axonal guidance molecules(eg Ephrins and Semaphorins) have been found in platlet synapse.In addition to axonal guidance,axonal guidance molecules have been shown to participate in the pathophysiological processes,including immune response,tumor metastasis,angiogenesis,and thrombosis. Most recently,it was found that deletion of a semaphorin family member,Sema4D,attenuated platelet hyperreactivity in the setting of dyslipidemia and protected from the development of atherosclerotic plaques.This article summarizes the progress in the understanding of the molecular mechanisms by which axonal guidance molecules affect atherothrombosis.

Abstract:Aim To observe the effects of high low density lipoprotein cholesterol (LDLC) and fluvastatin on PAC-1 and CD40L expression of platelets in vitro and vivo and investigate its mechanism. Methods In vivo experiments,before and after treatment of fluvastatin for high LDLC patients,the CD40L and PAC-1 positive rate of platelets by flow cytometry were examined under the same conditions. The CD40L and PAC-1 expression of each group were compared. In vitro experiments,after the co-incubation of these chosed plasma or LDLC with the same healthy platelets and the interference with fluvastatin,the PAC-1 and CD40L positive rate of platelets were tested by flow cytometry and platelets total CD40L protein content by Western blotting and CD40L mRNA were examined under the same conditions in all objects. The PAC-1 and CD40L positive rate,the total CD40L content and CD40L mRNA of each group were compared respectively. Results Not only in vivo study but also in vitro study,the platelet PAC-1 and CD40L positive rate in high LDLC group were significant higher than in control group(P all<0.01). Followed the LDLC concentration decrease,the platelet PAC-1 and CD40L positive rate decreased after the treatment of fluvastatin in vivo,but in vitro study,the fluvastatin didnt affect the expression significantly. LDLC itself didnt affect the platelet PAC-1 and CD40L positive rate in

Abstract:Aim To investigate the relationship between platelet CD62P and CD63 expression and acute cevebral infarction(ACI). Methods The expression of CD62P,CD63 was detected by flow cytometry in 61 patients with acute cevebral infarction(ACI),and 59 healthy control subjects. Results CD62P,CD63 in acute cevebral infarition were 6.26%±1.68% vs 2.32%±1.14%,6.14%±1.89% vs 2.88%±1.15% respectively,and the result has statistical significance compa with those of the control group(P><0.01). Conclusion The formation of thrombus in actute cerebral infaration patients is highly related to the platelets activation,which can be a diagnostic indicator of cevebral infarction disease.

Abstract:Aim To examine the relationship between glycopropean complex of activated platelet (PAC-1) and lipid metabolic disturbance in cases of type 2 diabetes mellitus (DM). Methods One hundred and twenty two patients with DM (type 2) were divided into lipid metabolic disturbance group (62 cases) and normal lipid metabolism group (58 cases). 25 normals were selected as the control. Flow-cytometry was used to detect the PAC-1 level and therefore the deference between the two groups was analysed. The correlation between triglyceride (TG), high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDLC) and PAC-1 was also evaluated. Results The PAC-1 level in type 2 DM cases was higher than that in control subjects. It was also markedly higher in abnormal lipid metabolic cases than that in normal lipid metabolic cases. LDLC correlated positively with PAC-1 (r=0.64, p<0.05). Conclusion Abnormal lipid metabolism is the main factor resulting in a high PAC-1 level.

Abstract:Aim To study the effect of hypercholesterolemia (HC) on platelet quantitative stereologic parameters and its change after treatment by pravastatin. Methods 20 patients with HC were selected and treated with pravastatin 10～20 mg/d for 4～8 weeks. The changes of platelet ultrastructure were observed by electron microscopic and analysed with quantitative stereologic method. Results After 4～8 weeks treatments, the levels of serum total cholesterol (TC) and platelet aggregation function were lowered and most of platelet quantitative stereologic parameters were improved. Conclusion Altered platelet function and quantitative stereologic parameters with pravastatin therapy in patients with HC can be corrective with its mechanism of enhancing atherosclerosis regression.