趋化因子CCL2对血小板p38MAPK-HSP27通路的影响

发布时间：2018-07-07 10:36

本文选题：趋化因子CCL + 心肌梗死　；参考：《解放军医学杂志》2017年05期

【摘要】：目的探讨CC趋化因子配体2(CCL2)在残余血小板高反应中的作用及其调控血小板的可能机制。方法纳入ST段抬高型心肌梗死(STEMI)患者40例,采用Verify Now法检测P2Y12反应单元(PRU),根据检测结果将40例患者分为残余血小板高反应组(高反应组,n=24)和残余血小板正常反应组(正常反应组,n=16)。ELISA检测两组患者血浆中CCL2的表达,Western blotting检测血小板中CCL2和CCR2的表达,ARY003B蛋白芯片筛选经外源性CCL2刺激后血小板中磷酸化水平发生变化的激酶。Western blotting验证经CCL2刺激,或经CCR2拮抗剂(RS 102895)、p38MAPK信号通路抑制剂(SB 203580)预处理后血小板中p38MAPK和HSP27的磷酸化变化。结果高反应组血浆中CCL2浓度、血小板中CCL2和CCR2表达均明显高于正常反应组。经外源性CCL2刺激后,芯片筛选发现p38α、HSP27的磷酸化水平增高。在CCL2刺激前,应用RS 102895或SB 203580预处理血小板,Western blotting检测显示p38MAPK和HSP27的磷酸化水平下降。结论 CCL2以自分泌/旁分泌的方式参与残余血小板高反应,CCL2可能通过p38MAPK-HSP27通路调控血小板。
[Abstract]:Objective to investigate the role of CC chemokine ligand 2 (CCL 2) in the hyperresponsiveness of residual platelet and its possible mechanism. Methods 40 patients with ST-segment elevation myocardial infarction (STEMI) were included. P2Y12 reaction unit (PRU) was detected by Verify now method. According to the results, 40 patients were divided into two groups: high response group (high response group) and normal reaction group (n = 16). Elisa was used to detect CCL2 in plasma of two groups. The expression of CCL2 and CCR2 in platelets was detected by Western blotting. The protein chip ARY003B was used to screen the kinase. Western blotting showed that the phosphorylation of platelet was stimulated by CCL2. Or the phosphorylation of p38 MAPK and HSP27 in platelets were pretreated with CCR2 antagonist (RS 102895) and p38 MAPK signaling pathway inhibitor (SB 203580). Results the levels of CCL2 in plasma and the expression of CCL2 and CCR2 in platelets in high response group were significantly higher than those in normal reaction group. After stimulation with exogenous CCL 2, the phosphorylation level of p38 伪 -HSP27 was found to be increased by microarray screening. Before CCL2 stimulation, the phosphorylation of p38 MAPK and HSP27 was decreased after pretreatment with RS 102895 or SB 203580. Conclusion CCL2 is autocrine / paracrine involved in the hyperresponsiveness of residual platelet. CCL2 may regulate platelet by p38MAPK-HSP27 pathway.
【作者单位】：沈阳军区总医院全军心血管病研究所;
【基金】：国家自然科学基金面上项目(81670340);国家自然科学基金青年项目(81500282)~~
【分类号】：R542.22

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