趋化因子SDF-1对巨噬细胞迁移和极化的调控作用  

The regulatory role of chemokine SDF-1 on macrophage migration and polarization

作　　者：陈欣欣 狄静怿 陈禹江 陈文霞[1,2] CHEN Xin-xin;DI Jing-yi;CHEN Yu-jiang;CHEN Wen-xia(College&Hospital of Stomatology,Guangxi Medical University,Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction,Guangxi Health Commission Key laboratory of prevention and treatment for oral infectious diseases,Nanning 530021,China;不详)

机构地区：[1]广西医科大学口腔医学院/附属口腔医院,广西口腔颌面修复与重建研究重点实险室,广西壮族自治区卫生健康委员会口腔感染性疾病防治重点实验室,广西南宁530021 [2]广西医科大学附属口腔医院牙体牙髓科,广西南宁530021

出　　处：《牙体牙髓牙周病学杂志》2024年第1期12-19,共8页Chinese Journal of Conservative Dentistry

基　　金：国家自然科学基金项目(82060201)。

摘　　要：目的:探讨基质细胞衍生因子-1(SDF-1)及其受体C-X-C趋化因子受体4(CXCR4),C-X-C趋化因子受体7(CXCR7)对巨噬细胞迁移和极化的调控作用。方法:Transwell检测SDF-1/CXCR4、SDF-1/CXCR7通路对巨噬细胞迁移能力的影响;Western blot检测SDF-1对CXCR4和CXCR7受体蛋白表达的影响;RT-qPCR、ELISA以及流式细胞术检测SDF-1/CXCR4、SDF-1/CXCR7通路对巨噬细胞极化的影响。结果:SDF-1可明显促进巨噬细胞迁移并促进CXCR4和CXCR7受体蛋白的表达(P<0.001);SDF-1的促进迁移作用可以被AMD3100和CXCR7 antagonist-1抑制(P<0.001);SDF-1可以增强M1型标记物TNF-α、iNOS和M2型标记物IL-10、TGF-β的表达(P<0.05),CXCR7 antagonist-1降低这些标记物的表达(P<0.01);AMD3100对SDF-1增强标记物表达作用无明显影响(P>0.05);流式细胞术结果表明,与对照组相比,SDF-1显著提高M2型的表达比例,该作用可被CXCR7 antagonist-1抑制。结论:SDF-1可以激活CXCR4/CXCR7信号通路,其促进巨噬细胞迁移作用通过CXCR4和CXCR7两个受体实现,而对巨噬细胞极化的调控主要是通过CXCR7受体发挥作用。AIM:To investigate the regulatory role of the chemokine SDF-1(Stromal cell-derived factor-1)and its receptors CXCR4(C-X-C chemokine receptor type4)and CXCR7(C-X-C Chemokine receptor type 7)on macrophage migration and polarization.METHODS:The effect of the SDF-1/CXCR4 and SDF-1/CXCR7 pathways on macrophage migration was assessed using Transwell assays;the influence of SDF-1 on the expression of CXCR4 and CXCR7 receptor proteins was examined by Western blot analysis;and the impact of SDF-1/CXCR4 and SDF-1/CXCR7 pathways on the regulation of macrophage polarization was measured using RT-qPCR,ELISA,and flow cytometry.RESULTS:SDF-1 significantly promoted macrophage migration and enhanced the expression of CXCR4 and CX-CR7 receptor proteins(P<0.001).The migration-promoting effect of SDF-1 could be inhibited by AMD3100 and CXCR7 antagonist-1(P<0.001).SDF-1 also increased the expression of M1 markers TNF-α,iNOS,and M2 markers IL-10,TGF-β(P<0.05),while CXCR7 antagonist-1 decreased the expression of these markers(P<0.01).AMD3100 had no significant effect on SDF-1-induced enhancement of marker expressions(P>0.05).Flow cytometry results indicated that compared to the control group,SDF-1 significantly increased the proportion of M2 type expression,and this effect could be suppressed by CXCR7 antagonist-1.CONCLUSION:SDF-1 can activate the CXCR4/CXCR7 signaling pathway,and its macrophage migration-promoting effects are achieved through both CXCR4 and CXCR7 receptors,while the regulation of macrophage polarization is mainly mediated by the CXCR7 receptor.

关 键 词：SDF-1 CXCR4 CXCR7 巨噬细胞 细胞迁移 巨噬细胞极化 

分 类 号：R78[医药卫生—口腔医学]