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首页|期刊导航|临床口腔医学杂志|LncRNA-TNFRSF13C调控miR-1246对LPS诱导的牙髓细胞HIF-1α及生物活性的影响

LncRNA-TNFRSF13C调控miR-1246对LPS诱导的牙髓细胞HIF-1α及生物活性的影响OACSTPCD

LncRNA-TNFRSF13C regulates the effects of miR-1246 on HIF-1α and bioactivity of LPS-induced dental pulp cells

中文摘要英文摘要

目的:探讨LncRNA-TNFRSF13C调控miR-1246 对脂多糖(lipopolysaccharides,LPS)诱导的牙髓细胞低氧诱导因子-1α(hypoxia-inducible factor 1α,HIF-1α)及生物活性的影响机制.方法:将人牙髓细胞(human dental pulp cells,HDPCs)经LPS处理后,分为HDPCs组、TNFRSF13C NC-siRNA组、TNFRSF13C-siRNA组、sno-TNFRSF13C组、miR-NC组、miR-1246 mimics组、miR-1246 siRNA组、TNFRSF13C-siRNA+miR-1246 siRNA组.qRT-PCR检测各组细胞LncRNA-TNFRSF13C、miR-1246 相对表达;免疫印迹检测各组细胞HIF-1α蛋白表达;CCK-8 检测各组细胞活性;流式细胞仪检测细胞凋亡率;茜素红染色观察细胞矿化情况.结果:与HDPCs组、TNFRSF13C NC-siRNA组相比,TNFRSF13C-siRNA组HIF-1α表达量、细胞凋亡率、LncRNA-TNFRSF13C表达降低,细胞增殖率升高(P<0.05).与miR-NC组相比,miR-1246 siRNA组 HIF-1α 表达量、细胞凋亡率、miR-1246 表达水平降低,细胞增殖率升高(P<0.05).与TNFRSF13C-siRNA组、miR-1246 siRNA组相比,TNFRSF13C-siRNA+miR-1246 siRNA组HIF-1α表达量、细胞凋亡率降低,细胞增殖率升高(P<0.05).TNFRSF13C-siRNA组、miR-1246 siRNA组存在更多的矿化结节及不透光致密影;TNFRSF13C-siRNA+miR-1246 siRNA组存在大量矿化结节,致密深染.结论:抑制LncRNA-TNFRSF13C对LPS处理的HDPCs具有促进活性,降低凋亡的作用,促进HDPCs矿化,同时也可抑制HIF-1α,研究机制与调控miR-1246 活性相关.

Objective:To investigate the effect of LncRNA-TNFRSF13C regulation of miR-1246 on hypoxia-inducible factor 1α(HIF-1α)and bioactivity of lipopolysaccharides(LPS)-induced dental pulp cells.Methods:After human dental pulp cells(HDPCs)treated with LPS,they were divided into HDPCs group,TNFRSF13C NC-siRNA group,TNFRSF13C-siRNA group,sno-TNFRSF13C group,miR-NC group,miR-1246 mimics group,and miR-1246 siRNA group,TNFRSF13C-siRNA+miR-1246 siRNA group.The relative expressions of LncRNA-TNFRSF13C and miR-1246 were detected by qRT-PCR.The expression of HIF-1α was detected by Western blotting.CCK-8 was used to detect cell activity in each group.The apoptosis rate was detected by flow cytometry.The mineralization of cells was observed by alizarin red staining.Results:Com-pared with HDPCs group and TNFRSF13C NC-siRNA group,HIF-1α expression,apoptosis rate and LncRNA-TNFRSF13C expression in TNFRSF13C-SiRNA group were significantly decreased,and cell proliferation rate was significantly increased(P<0.05).Compared with miR-NC group,HIF-1α expression,cell apoptosis rate and expression level of miR-1246 in miR-1246 siRNA group were significantly decreased,and cell proliferation rate was significantly increased(P<0.05).Compared with TNFRSF13C-siRNA group and miR-1246 siRNA group,HIF-1α expression,cell apoptosis rate in TNFRSF13C-siRNA+ miR-1246 siRNA group were significantly decreased,cell proliferation rate was significantly increased(P<0.05).TN-FRSF13C-siRNA group and miR-1246 siRNA group had more mineralized nodules and dense mass.The TNFRSF13C-siRNA+ miR-1246 siRNA group had a large number of mineralized nodules,which were dense and deeply stained.Conclusion:Inhi-bition of LncRNA-TNFRSF13C can promote the activity of LPS-treated HDPCs,reduce the effect of apoptosis,promote the mineralization of HDPCs,and inhibit HIF-1α.The study mechanism is related to the regulation of miR-1246 activity.

张雪;任燕;白静;李月辉

唐山中心医院 河北 唐山 063000唐山市丰润区人民医院 河北 唐山 063000开滦(集团)有限责任公司唐家庄医院 河北 唐山 063100

口腔医学

牙髓炎牙髓细胞脂多糖miR-1246LncRNA-TNFRSF13C

PulpitisDental pulp cellsLipopolysaccharidemiR-1246LncRNA-TNFRSF13C

《临床口腔医学杂志》 2024 (005)

263-268 / 6

河北省医学科学基金资助项目(编号:20230240)

10.3969/j.issn.1003-1634.2024.05.003

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