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作 者:董丽宏[1] 朱晓琳[1] 赵海燕[1] 何辰[1] Dong Lihong;Zhu Xiaolin;Zhao Haiyan(Department of Critical Care Medicine,First Affiliated Hospital of Kunming Medical University,Kunming 650032)
机构地区:[1]昆明医科大学第一附属医院重症医学科,昆明650032
出 处:《现代妇产科进展》2020年第6期416-420,共5页Progress in Obstetrics and Gynecology
摘 要:目的:探讨miR-26a在妊娠期高血压疾病患者中的表达及其对滋养层细胞侵袭和凋亡的影响及其机制。方法:qRT-PCR法检测miR-26a表达,miRNA转染JAR细胞系构建control、miR-26a NC、miR-26、miR-26a inhibitor NC和miR-26a inhibitor组细胞。CCK-8法检测细胞活力,Brdu检测细胞增殖,Matrigel侵袭实验检测细胞侵袭,TUNEL检测细胞凋亡,Western blot法检测Bcl-2、Bax、Cleaved-caspase 9、E-cadherin、Vimentin表达。结果:妊娠期高血压疾病孕妇血浆中miR-26a表达量明显高于正常孕妇,差异有统计学意义(P<0.05)。过表达miR-26a抑制JAR细胞活力、增殖与侵袭能力(P<0.05);抑制miR-26a表达则增加JAR细胞活力、增殖与侵袭能力(P<0.05)。过表达miRNA-26后,抗凋亡蛋白Bcl-2表达量下降(P<0.05),凋亡蛋白Cleaved Caspase-9和Bax表达量升高(P<0.05);抑制miRNA-26表达后,抗凋亡蛋白Bcl-2表达量增加(P<0.05),凋亡蛋白Cleaved Caspase-9和Bax表达减少(P<0.05)。结论:miR-26a在妊娠期高血压疾病患者中高表达,过表达miR-26a能抑制滋养层细胞细胞增殖和侵袭,促进凋亡,其可能机制是通过抑制EMT,调节Bcl-2/Caspase-9介导的。Objective:To investigate the expression of miR-26 a in patients with PIH during pregnancy compared with normal controls.Subsequently,the effects and mechanism of miR-26 a on invasion and apoptosis of human choriocarcinoma(JAR)cells were investigated.Methods:Quantitative RT-PCR analysis was used to determine the expression of miR-26 a.Transfect JAR cell by miRNA to establish control,miR-26 a NC,miR-26,miR-26 a inhibitor NC and miR-26 a inhibitor group cell.CCK-8 method was used to examine metabolic activity,Brdu assay was used to reflect the proliferation of the cells.Invasion was observed bymatrigel-coated transwells.Apoptosis rate was measured by TUNEL staining.The Bcl-2,Bax,Cleaved-caspase 9,E-cadherin and Vimentin were detected by Western blot.Results:The expression of miR-26 a was upregulated in patients with PIH compared with controls.Overexpression of miR-26 a suppressed the JAR cell proliferation and invasion.However,blocking of miR-26 a promoted proliferation and invasion.Overexpression of miR-26 a induced cell apoptosis,blocking of miR-26 a inhibited cell apoptosis.Overexpression of miR-26 a decreased anti-apoptotic protein Bcl-2 and Vimentin expression,increased Bax,Cleaved Caspase-9,and E-cadherin level than control.Blocking of miR-26 a increased Bcl-2 protein and Vimentin level,decreased the level of Bax,Cleaved caspase-9 and E-cadherin.Conclusion:The expression of miR-26 a is up-regulated in patients with pre-eclampsia,and miR-26 a overexpression suppressed the cell proliferation and invasion,and promoting cell apoptosis through regulating the EMT and Bcl-2/caspase 9 pathway.
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