文章摘要
程 华,金梅花,董俭达.缺血再灌注条件下内皮祖细胞促进单核/巨噬细胞向M1型极化的研究[J].南京医科大学学报,2020,(2):180~184
缺血再灌注条件下内皮祖细胞促进单核/巨噬细胞向M1型极化的研究
The role and mechanism of endothelial progenitor cells to promote mononuclear/macrophage to type M1 polarization under ischemic reperfusion
投稿时间:2019-07-17  
DOI:10.7655/NYDXBNS20200206
中文关键词: 内皮祖细胞  缺血再灌注  单核/巨噬细胞  心血管疾病
英文关键词: endothelial progenitor cells  ischemia⁃reperfusion  mononuclear/macrophage  cardiovascular disease
基金项目:宁夏回族自治区重点研发计划项目(2018EBG02006)
作者单位
程 华 宁夏医科大学总医院心血管内科 宁夏 银川 750000 
金梅花 宁夏医科大学总医院心血管内科 宁夏 银川 750000 
董俭达 宁夏医科大学病理学系 宁夏 银川 750004 
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中文摘要:
      目的:探讨在缺血再灌注条件下内皮祖细胞(endothelial progenitor cell,EPC)促进单核/巨噬细胞向M1型极化的作用及机制。方法:获取健康志愿者的外周血,原代培养EPC和单核/巨噬细胞;体外构建细胞缺血再灌注损伤模型;流式细胞术检测EPC表面细胞间黏附分子?1(intercellular adhesion molecule ?1,ICAM?1)、血管细胞黏附分子?1(vascular cell adhesion molecule?1,VCAM?1)和E?选择素的表达;ELISA检测上清中ICAM?1、VCAM?1和E?选择素浓度;采用Transwell小室进行EPC和单核/巨噬细胞共培养,流式细胞术检测M1和M2型单核/巨噬细胞比例。结果:缺血再灌注条件下EPC表面表达及其分泌ICAM?1和VCAM?1均没有显著变化,两组之间差异均没有统计学意义;对照组EPC表面E?选择素平均荧光强度为10.89,缺血再灌注组为33.93(t=3.895,P=0.018);对照组EPC上清中E?选择素浓度为3.69 ng/mL,缺血再灌注组为18.17 ng/mL(t=4.568,P=0.010);缺血再灌注条件下EPC能够促进单核/巨噬细胞向M1型极化,对照组M1型单核/巨噬细胞比例为58.83%,缺血再灌注组为81.43%(t=5.394,P=0.006),E?选择素阻断能抑制这种作用(t=5.950,P=0.004);缺血再灌注条件下EPC抑制单核/巨噬细胞向M2型极化,对照组M2型单核/巨噬细胞比例为60.57%,缺血再灌注组为35.30%(t=6.424,P=0.003),E?选择素阻断能抑制这种作用(t=4.179,P=0.014)。结论:在缺血再灌注损伤条件下,EPC能够通过高表达和分泌E?选择素,促进单核/巨噬细胞向M1型极化,为缺血再灌注损伤的治疗提供了新的靶点。
英文摘要:
      Objective:This study aims to explore the role and mechanism of endothelial progenitor cells(EPC) promoting monocyte/macrophage to type M1 polarization under ischemia and reperfusion. Methods:the peripheral blood of healthy volunteers was obtained,the primary EPC and mononuclear/macrophage were cultured. The model of cell ischemia?reperfusion injury was established in vitro,and the expression of intercellular adhesion molecule ?1(ICAM?1),vascular cell adhesion molecule ?1(VCAM?1)and E? selectin on EPC surface were detected by flow cytometry. ELISA was used to detect the concentration of ICAM?1,VCAM?1 and E? selectin in the supernatant. Co?culture of EPC and mononuclear/macrophages was performed by Transwell chamber,and the ratio of M1 to M2 type monocytes/macrophages was detected by flow cytometry. Results:There was no significant change in the expression and the secretion of ICAM?1 and VCAM?1 of EPC under the ischemic reperfusion condition,and there was no significant difference between the two groups. The average fluorescence intensity of E? selectin on the surface of EPC was 10.89 in the control group and 33.93 in the ischemia reperfusion group(t=3.895,P=0.018). The concentration of E? selectin in the EPC supernatant was 3.69 ng/mL in the control group and 18.17 ng/mL in the ischemia?reperfusion group(t=4.568,P=0.010). Under ischemia reperfusion condition,EPC promoted monocyte/macrophage to M1 type polarization. The proportion of monocyte/macrophage type M1 was 58.83% in control group and was 81.43% in ischemia reperfusion group(t=5.394,P=0.006),E? selectin blockage could inhibit this effect(t=5.950,P=0.004). Under ischemia reperfusion condition,EPC inhibited monocyte/macrophage to M2 type polarization. The ratio of M2 monocyte/macrophage was 60.57% in control group and was 35.30% in ischemia reperfusion group(t=6.424,P=0.003),E? selectin blockage could inhibit this effect(t=4.179,P=0.014). Conclusion:Under the condition of ischemia?reperfusion injury,EPC can promote the monocyte/macrophage to M1 polarization through the high expression and secretion of E? selectin. Our research provides a new target for the treatment of ischemia?reperfusion injury.
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