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目的探讨骨髓间充质干细胞(BMSCs)连接蛋白43(Cx43)表达对多发性骨髓瘤(MM)RPMI 8226细胞耐药的影响。方法体外分离、培养BMSCs,采用RT-PCR法检测BMSCs、RPMI 8226细胞Cx43的表达,流式细胞术和多重液相蛋白定量技术分别检测BMSCs与RPMI 8226细胞共培养对RPMI 8226细胞凋亡和细胞因子分泌的影响。结果 BMSCs及RPMI 8226细胞均表达Cx43。BMSCs与RPMI 8226细胞共培养后,上清液中IL-6、IL-10和TGF-β水平增加,硼替佐咪诱导的RPMI 8226细胞凋亡作用减弱;而细胞间隙连接通讯(GJIC)特异性阻断剂18α甘草次酸(18α-GA)能明显逆转上述观察指标的改变过程。结论 BMSCs与RPMI 8226细胞间可形成功能性GJIC,是BMSCs促进MM细胞生存及介导其耐药的重要原因之一。
Objective To investigate the effect of connexin 43 (Cx43) expression of bone marrow mesenchymal stem cells (BMSCs) on the drug resistance of multiple myeloma (MM) RPMI 8226 cells. Methods BMSCs were isolated and cultured in vitro. The expression of Cx43 in BMSCs and RPMI 8226 cells was detected by RT-PCR, and the effects of BMSCs and RPMI 8226 cells co-cultured on RPMI 8226 cells were detected by flow cytometry and multiple liquid protein quantification. The impact of factor secretion. Results Both BMSCs and RPMI 8226 cells expressed Cx43. After co-cultured with BMSCs and RPMI 8226 cells, the levels of IL-6, IL-10 and TGF-β increased in the supernatant and the apoptosis of RPMI 8226 cells induced by bortezomib decreased. However, the specificity of GJIC Blockade 18α glycyrrhetinic acid (18α-GA) can significantly reverse the changes in the above indicators. Conclusions Functional GJIC can be formed between BMSCs and RPMI 8226 cells, which is one of the important reasons that BMSCs promote the survival of MM cells and mediate their drug resistance.