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首页> 外文期刊>Journal of biomedical materials research. Part B, Applied biomaterials. >The induction of CXCR4 expression in human osteoblast‐like cells (MG63) by CoCr particles is regulated by the PLC‐DAG‐PKC pathway
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The induction of CXCR4 expression in human osteoblast‐like cells (MG63) by CoCr particles is regulated by the PLC‐DAG‐PKC pathway

机译：COCR颗粒的人骨细胞样细胞（Mg63）中CXCR4表达的诱导由PLC-DAG-PKC途径调节

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Abstract Background Osteolysis which leads to aseptic loosening of implants is a fundamental problem in joint replacement surgery (arthroplasty) and the leading cause for implant failure and revision surgery. Metal (CoCr) particles separated from implants by wear cause osteolysis and the failure of orthopedic implants, but the molecular mechanism is not clear. The chemokine receptor CXCR4 has been shown to play a pivotal role in periprosthetic osteolysis. The aim of this study was to determine which signal transduction pathway (PLC‐DAG‐PKC or MAPK/ERK) induces CXCR4 expression in osteoblast‐like cells (MG63) cells. Methods MG63 and Jurkat cells were stimulated with different amounts of particles (10 7 , 10 6 , and 10 5 ) for different time periods (30 min to 24 h), in the presence and absence of specific inhibitors (chelerythrine for the PLC‐DAG‐PKC pathway and PD98059 for the MAPK/ERK pathway). The expression of CXCR4‐specific mRNA was determined by real‐time polymerase chain reaction (PCR), and the PKC activity was measured by Western Blot using an antibody specific for PKC‐related phosphorylation. Results Real‐time PCR data showed that CXCR4 mRNA expression in MG63 cells induced by CoCr particles was significantly diminished by the PKC‐specific inhibitor chelerythrine. This effect was not observed with the MAPK/ERK inhibitor PD98059. The involvement of PKC was also confirmed by an intensified phosphorylation pattern after stimulation with CoCr particles. In Jurkat cells, none of the inhibitors exhibited any effect. Conclusion The induction of CXCR4‐specific mRNA expression in MG63 cells after stimulation with CoCr particles is regulated by the PLC‐DAG‐PKC pathway and not by the MAPK/ERK pathway. ? 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 105B: 2326–2332, 2017.
机译：摘要背景骨溶解，导致植入物的无菌松动是关节置换手术（关节成形术）和植入失败和修正手术的主要原因。金属（COCR）通过磨损分离植入物的颗粒，原因骨解和骨科植入物的失效，但分子机制尚不清楚。趋化因子受体CXCR4已被证明在骨髓溶质溶解中起着枢轴作用。该研究的目的是确定哪种信号转导途径（PLC-DAG-PKC或MAPK / ERK）在成骨细胞样细胞（MG63）细胞中诱导CXCR4表达。方法在存在和不存在特异性抑制剂（PLC-DAG的情况下，用不同的时间段（107,106和10 5）用不同的颗粒（107,106和10 5）刺激MG63和Jurkat细胞以不同的时间段（30分钟至24小时）刺激（30分钟至24小时）（PLC-DAG的Chelerythrine -PKC路径和MAPK / ERK路径的PD98059）。通过实时聚合酶链反应（PCR）测定CXCR4特异性mRNA的表达，并且使用针对PKC相关磷酸化的抗体的抗体测量PKC活性。结果实时PCR数据显示，COCR颗粒诱导的Mg63细胞中的CXCR4 mRNA表达被PKC特异性抑制剂培养梭菌显着减少。用MAPK / ERK抑制剂PD98059未观察到这种效果。在用Cocr颗粒刺激后，还通过强化磷酸化图案证实了PKC的参与。在Jurkat细胞中，没有一种抑制剂表现出任何影响。结论PLC-DAG-PKC途径对COCR颗粒刺激后MG63细胞CXCR4特异性mRNA表达的诱导，不由MAPK / ERK途径调节。还2016 Wiley期刊，Inc .J生物保解员B：Appl Biomater，105B：2326-2332,2017。

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