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FPR2通过ERK1/2信号通路调控炎症状态下滋养细胞生物学功能 被引量:5

Effect of FPR2 on regulation of trophoblast biological function in inflam⁃mation through ERK1/2 signaling pathway
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摘要 目的:明确甲酰肽受体2(FPR2)在炎症状态下对滋养细胞生物学功能的影响,分析其在绒毛膜羊膜炎中的作用,并探讨其机制。方法:收集10例绒毛膜羊膜炎患者和10例正常产妇的胎盘组织,利用免疫组化和Westernblot检测胎盘组织中FPR2的定位和表达。应用脂多糖(LPS)建立人绒毛膜滋养层细胞系HTR-8/SVneo体外炎症模型,利用Westernblot检测FPR2表达;应用小干扰RNA敲减FPR2基因,检测正常组、LPS处理组和LPS+FPR2敲减组细胞培养液上清中促炎因子白细胞介素6(IL-6)、IL-1β和肿瘤坏死因子α(TNF-α)的水平,并通过EdU实验、流式细胞术、Transwell实验和划痕实验检测细胞增殖、凋亡、侵袭和迁移;利用Westernblot分析丝裂原活化蛋白激酶(MAPK)信号通路中关键因子细胞外信号调节激酶1/2(ERK1/2)、p-ERK1/2、c-Jun氨基末端激酶(JNK)、p-JNK、p38和p-p38蛋白表达。结果:绒毛膜羊膜炎患者胎盘组织中FPR2表达显著增加(P<0.01)。FPR2敲减显著降低LPS诱导的HTR-8/SVneo细胞IL-6、IL-1β和TNF-α的分泌(P<0.01或P<0.05),同时减弱了LPS对HTR-8/SV⁃neo细胞增殖、凋亡、迁移和侵袭的影响(P<0.05或P<0.01);LPS激活了ERK1/2、JNK和p38信号通路(P<0.05或P<0.01),FRP2敲减后JNK和p38信号通路无显著变化,ERK1/2信号通路受到显著抑制(P<0.01)。结论:FPR2参与了炎症状态下滋养细胞功能的调节,其作用机制可能与ERK1/2信号通路有关。 AIM:To investigate the effect of formyl peptide receptor 2(FPR2)on the biological function of trophoblast in inflammation,amd to analyze its role in chorioamnionitis(CAM)and the mechanism.METHODS:The placental tissues were collected from 10 CAM patients and 10 normal pregnant women,and the location and expression of FPR2 in placenta were detected by immunohistochemical staining and Western blot.The in vitro inflammation model in hu-man trophoblast cell line HTR-8/SVneo was induced by lipopolysaccharide(LPS),and the expression of FPR2 was detected by Western blot.The FPR2 was knocked down by transfection of siRNA into HTR-8/SVneo cells.The concentrations of pro-inflammatory cytokines interleukin-6(IL-6),IL-1βand tumor necrosis factor-α(TNF-α)in the cell culture superna-tants of normal group,LPS group and LPS+siFPR2 group were detected by ELISA.The proliferation,apoptosis,migration and invasion of the cells were detected by EdU experiment,flow cytometry,Transwell invasion assay and wound healing assay.Western blot was implemented to analyze the protein levels of extracellular signal-regulated kinase 1/2(ERK1/2),p-ERK1/2,c-Jun N-terminal kinase(JNK),p-JNK,p38 and p-p38 in mitogen-activated protein kinase(MAPK)signaling pathway.RESULTS:The expression of FPR2 increased in the placenta of CAM patients(P<0.01).Knockdown of FPR2 decreased the release of IL-6,IL-1βand TNF-α,improved the proliferation,migration and invasion,and increased the apoptosis of HTR-8/SVneo cells treated with LPS(P<0.05 or P<0.01).The ERK1/2,JNK and p38 signaling path-ways were activated in LPS-treated HTR-8/SVneo cells(P<0.05 or P<0.01).No significant changes were detected in JNK and p38 signaling pathway after FPR2 was knocked down,while ERK1/2 signaling pathway was inhibited significant-ly(P<0.01).CONCLUSION:The FPR2 was involved in the regulation of trophoblast function in inflammation,and its mechanism may be related to ERK1/2 signaling pathway.
作者 李淑贤 周美娟 李安娜 房振亚 郭君君 张美华 LI Shu-xian;ZHOU Mei-juan;LI An-na;FANG Zhen-ya;GUO Jun-jun;ZHANG Mei-hua(Key Laboratory of Birth Regulation and Control Technology of National Health Commission of China,Maternal and Child Health Care Hospital of Shandong Province,Jinan 250014,China)
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2022年第8期1478-1486,共9页 Chinese Journal of Pathophysiology
基金 山东省自然科学基金面上项目(No.ZR2021MH262) 山东省医药卫生科技发展计划项目(No.202005021516)。
关键词 绒毛膜羊膜炎 甲酰肽受体2 炎症 ERK1/2信号通路 Chorioamnionitis Formyl peptide receptor 2 Inflammation ERK1/2 signaling pathway
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