LncRNA MINCR在牙髓炎中通过p38 MAPK信号通路对中性粒细胞存活、迁移、凋亡及炎症因子产生的影响OA
The effect of lncRNA MINCR on neutrophil survival,migration,apoptosis,and inflammatory cytokine produc-tion in pulpitis via the p38 MAPK signaling pathway
目的:探究 MYC 诱导的长链非编码 RNA(MYC-induced long non-coding RNA,MINCR)在牙髓炎中通过p38 丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路对中性粒细胞存活、迁移、凋亡及炎症因子产生的影响.方法:采用 2 μg/mL 脂多糖(lipopolysaccharide,LPS)处理人牙髓成纤维细胞,将其与人外周血中分离的中性粒细胞建立共培养体系,将中性粒细胞分为阴性对照短发夹 RNA 组(sh-NC 组)载体、MINCR 短发夹 RNA组(sh-MINCR 组)、阴性对照过表达组(NC-OE 组)、MINCR 过表达组(MINCR-OE 组)、MINCR 过表达+p38 抑制物组(MINCR-OE+p38 inhibitor 组),qRT-PCR 检测各组细胞 MINCR 表达,Western blot 检测磷酸化(p)-p38 MAPK 蛋白表达;CCK-8法与 Transwell 小室检测各组细胞存活与迁移,Annexin V-PE/7-AAD 双染色法和半胱氨酸天冬氨酸蛋白酶-3(cysteine-aspartic acid protease 3,Caspase-3)活性检测试剂盒检测细胞凋亡,ELISA 法检测 IL-1β、TNF-α 和 IL-6 水平.结果:LPS 处理人牙髓成纤维细胞与中性粒细胞共培养后,可提高中性粒细胞 MINCR 与 p-p38 MAPK 蛋白表达(P<0.05).沉默 MINCR 表达可显著降低中性粒细胞存活、迁移及炎症因子水平,增加细胞凋亡,抑制 p-p38 MAPK蛋白表达(P<0.05);过表达 MINCR 可显著增加中性粒细胞存活、迁移及炎症因子水平,降低细胞凋亡,促进 p-p38 MAPK 蛋白表达(P<0.05);抑制 p-p38 MAPK 蛋白表达可逆转过表达 MINCR 对中性粒细胞存活、迁移、凋亡及炎症因子水平的影响(P<0.05).结论:MINCR 在牙髓炎中通过促进 p38 MAPK 信号通路影响中性粒细胞存活、迁移、凋亡及炎症因子产生.
Objective:To explore the effect of MYC-induced long non-coding RNA(MINCR)on neutrophil survival,migration,apoptosis,and cytokine production in pulpitis via the p38 mitogen-activated protein kinase(MAPK)signaling path-way.Methods:Human dental pulp fibroblasts were treated with 2 μg/mL lipopolysaccharide(LPS)and co-cultured with neu-trophils isolated from human peripheral blood.The neutrophils were divided into negative control short hairpin RNA group(sh-NC group),MINCR short hairpin RNA group(sh-MINCR group),negative control overexpression group(NC-OE group),the MINCR overexpression group(MINCR-OE group),and the MINCR overexpression+p38 inhibitor group(MINCR-OE+p38 inhibitor group).qRT-PCR was used to detect MINCR expression in cells from each group.Western blot was per-formed to detect phosphorylated(p)-p38 MAPK protein expression.CCK-8 method and Transwell chamber were used to de-tect cell viability and migration in cells from each group.Annexin V-PE/7-AAD double staining and cysteine-aspartic acid protease 3(Caspase-3)activity assay kit were performed to detect cell apoptosis.ELISA method was used to measure the lev-els of IL-1β,TNF-α,and IL-6.Results:After co-culture of LPS-treated human dental pulp fibroblasts with neutrophils,the expression of MINCR and p-p38 MAPK protein was significantly increased in neutrophils(P<0.05).Silencing MINCR ex-pression significantly reduced neutrophil viability,migration,and inflammatory factors,increased cell apoptosis,and inhibited p-p38 MAPK protein expression(P<0.05).Overexpression of MINCR significantly enhanced neutrophil viability,migration,and inflammatory factors,reduced cell apoptosis,and promoted p-p38 MAPK protein expression(P<0.05).Inhibition of p-p38 MAPK protein expression could reverse the effect of MINCR overexpression on neutrophil viability,migration,apoptosis,and inflammatory factors(P<0.05).Conclusion:MINCR influences neutrophil survival,migration,apoptosis,and the produc-tion of inflammatory factors in pulpitis by promoting the p38 MAPK signaling pathway.
张叶影;刘远航;郑欣欣;宋璨;梁晓龙
石家庄市第二医院口腔科 河北 石家庄 050000石家庄市第二医院口腔科 河北 石家庄 050000石家庄市第二医院口腔科 河北 石家庄 050000石家庄市第二医院口腔科 河北 石家庄 050000石家庄市第二医院口腔科 河北 石家庄 050000
医药卫生
MYC诱导的长链非编码RNA牙髓炎p38丝裂原活化蛋白激酶中性粒细胞共培养体系
MYC-induced long non-coding RNAPulpitisp38 mitogen-activated protein kinaseNeutrophilsCo-culture system
《临床口腔医学杂志》 2026 (5)
259-264,6
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