干扰趋化因子CC受体-2调控p38MAPK信号通路抑制人口腔黏膜上皮细胞系增殖的机制

发布时间：2018-05-16 12:43

本文选题：趋化因子CC受体- + 口腔黏膜下纤维性变　；参考：《中国老年学杂志》2017年23期

【摘要】：目的探讨干扰趋化因子CC受体(CCR)2基因的表达对口腔黏膜上皮细胞增殖的影响及机制。方法 Western印迹检测CCR2在口腔黏膜下纤维性变(OSF)中的表达;用CCR2的siRNA转染人口腔黏膜上皮细胞系(HOMC)细胞,转染48 h后用Western印迹检测各组细胞中CCR2蛋白表达;细胞增殖与活性检测(CCK8)实验检测细胞增殖;Western印迹检测p38丝裂原活化蛋白激酶(p38MAPK)、磷酸化(p)-p38MAPK蛋白表达。结果 CCR2在OSF组织中的表达显著高于正常口腔黏膜组织(P0.01);阴性对照(NC)-siRNA组CCR2蛋白表达、细胞存活率及p38MAPK、p-p38MAPK蛋白表达与对照组比较差异无统计学意义(P0.05);CCR2-siRNA组CCR2蛋白表达、细胞存活率及p-p38MAPK蛋白表达均显著低于对照组(P0.01)。结论 CCR2在OSF中高表达,抑制CCR2的表达可通过调控p38MAPK信号通路抑制HOMC的增殖。
[Abstract]:Objective to investigate the effect and mechanism of CCR2 gene expression on the proliferation of oral mucosal epithelial cells (OMECs). Methods Western blot was used to detect the expression of CCR2 in oral submucosal fibrotic degeneration (OSF), and CCR2 siRNA was used to transfect human oral mucosal epithelial cell line (Hom). After 48 h of transfection, the expression of CCR2 protein was detected by Western blotting. The expression of p38 mitogen-activated protein kinase (p38 MAPK) and phosphorylated pP38 MAPK protein was detected by Western blotting. Results the expression of CCR2 in OSF was significantly higher than that in normal oral mucosa (P 0.01), but the expression of CCR2 protein, cell survival rate and p38 MAPK p-p38 MAPK protein in the negative control group were not significantly different from those in the control group. There was no significant difference in the expression of CCR2 protein in the CCR2-siRNA group. The cell survival rate and the expression of p-p38MAPK protein were significantly lower than those of the control group (P 0.01). Conclusion the high expression of CCR2 in OSF and the inhibition of CCR2 expression can inhibit the proliferation of HOMC by regulating the p38MAPK signaling pathway.
【作者单位】：南阳医学高等专科学校第一附属医院口腔科;郑州大学第一附属医院郑州大学口腔医学院;延边大学医学院病理学教研部;
【基金】：吉林省教育厅“十三五”科学技术研究项目(吉教科合字[2016]第266号)
【分类号】：R781.5

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