首页|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

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

PulpitisDental pulp cellsLipopolysaccharidemiR-1246LncRNA-TNFRSF13C

张雪、任燕、白静、李月辉

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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

牙髓炎 牙髓细胞 脂多糖 miR-1246 LncRNA-TNFRSF13C

河北省医学科学基金

20230240

2024

临床口腔医学杂志
华中科技大学同济医学院附属同济医院,中华口腔医学会口腔黏膜病专业委员会 中华医学会武汉分会

临床口腔医学杂志

CSTPCD
影响因子:0.783
ISSN:1003-1634
年,卷(期):2024.40(5)
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