Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNA...Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BIM）, calmodulin-dependent protein kinase IIδ（CaMKIIδ） and Cyclophilin D （CypD）. Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR （qPCR） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected展开更多
Objective: Emerging evidence indicates that long non-coding RNAs(lnc RNAs) are critical in carcinogenesis and progression of ovarian cancer. This study aimed to explore the functions and molecular mechanisms of plasma...Objective: Emerging evidence indicates that long non-coding RNAs(lnc RNAs) are critical in carcinogenesis and progression of ovarian cancer. This study aimed to explore the functions and molecular mechanisms of plasmacytoma variant translocation I(PVT1) in ovarian cancer Methods: PVT1 and miR-214 were detected by qRT-PCR assays in ovarian cancer tissues and cells. The cell proliferation,migration, and invasion abilities were detected by cell functional experiments, respectively. Western blot assay was performed to detect epithelial-mesenchymal transition(EMT) markers. MiR-214 expression regulated by PVT1 was studied by RNA immunoprecipitation(RIP) and chromatin immunoprecipitation(Ch IP) assays.Results: The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines. Elevated PVT1 expression was associated with advanced stage and indicated poor prognosis for ovarian cancer patients. The knockdown of PVT1 impaired SKOV3 cell proliferation, migration, and invasion in vitro. The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.Conclusions: PVT1 plays an important role in ovarian cancer tumorigenesis, which might be as a novel diagnostic marker and therapeutic target for ovarian cancer.展开更多
Objective:To explore the role of miR-214 in the progression of hepatocellular carcinoma（HCC） and its inhibitory mechanisms in depressing the signaling pathway of j3-catenin.this study was conducted.Methods:We ectopi...Objective:To explore the role of miR-214 in the progression of hepatocellular carcinoma（HCC） and its inhibitory mechanisms in depressing the signaling pathway of j3-catenin.this study was conducted.Methods:We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2.Differences between the two cell lines were compared in cell growth,proliferation,colony forming ability and cell cycles.RT-PCR method was applied for the quantification of β-catenin mRNA expression.Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets（ie.Cyclin D1,c-Myc and TCF-1）.The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression.Results:In comparison with negative（Lv-control-HepG2） and blank（HepG2） control,a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48<sup>7</sup>2h of cell culture experiments（P【0.05）.The miR-214 treatment resulted in a colony forming efficiency of（23.28±3.26）%,which was significantly lower than that of negative control[（51.31±3.97）%]（P【0.05）.According to FCM results,the experimental group,compared with control,showed a higher proportion of cells in G<sub>0</sub>/G<sub>1</sub> phase[（70.32±3.12）%]but a lower proportion in S phase[（18.42±2.90）%]（P【0.05）.The MTT assay demonstrated a significant inhibition of the proliferation and β-catenin expression of HCC cells compared with control（P【0.05）.while no significant difference was observed after HCC cells being transfected withβ-catenin overexpression plasmid（P】0.05）.By comparing to the RT-PCR and Western-blot results of control,the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression（P】0.05）.but an extremely inhibition in the protein level of β-catenin and its downstream targets Cyclin Dl,c-Myc.and TCF-1（P【0.05）.Conclusions:miR-214 functions a展开更多
目的:观察8周随意跑轮运动预适应对葡聚糖硫酸钠(DSS)诱导的C57BL/6小鼠实验性溃疡性结肠炎(UC)的影响,并探讨miR-214/PTEN信号环路在其间的可能作用机制。方法:40只雄性C57BL/6小鼠随机分为4组:安静组对照组(SED-CON)、安静组造模组(SE...目的:观察8周随意跑轮运动预适应对葡聚糖硫酸钠(DSS)诱导的C57BL/6小鼠实验性溃疡性结肠炎(UC)的影响,并探讨miR-214/PTEN信号环路在其间的可能作用机制。方法:40只雄性C57BL/6小鼠随机分为4组:安静组对照组(SED-CON)、安静组造模组(SED-DSS)、运动对照组(EXE-CON)、运动造模组(EXE-DSS)。SED-CON组和SED-DSS组大鼠安静饲养8周,EXE-CON组和EXE-DSS组进行8周随意跑轮运动。随后各造模组自由饮用3.5%DSS溶液诱导小鼠UC模型,各对照组自由饮用同等量的蒸馏水。每天观察并记录体重和疾病活动指数(DAI),7天后处死小鼠,取结肠观察组织病理学变化并进行组织损伤评分,检测IL-1β、IL-6、TNF-α、miR-214、PTEN、STAT3和Akt基因表达量以及NF-κB活性。结果:与SED-DSS组比较,EXE-DSS组小鼠临床症状改善(即体重增加、DAI降低、促炎症因子表达下调、结肠组织损伤减轻)。分子生物学测定发现:与SED-DSS组比较,EXE-DSS组miR-214,Akt、STAT3、IL-6表达量以及NF-κB活性降低(P<0.05),PTEN m RNA和蛋白表达量升高(P<0.05)。结论:长期随意跑轮运动预适应能够对DSS诱导的C57BL/6小鼠实验性UC起保护效应,其机制可能与部分恢复miR-214/PTEN信号环路功能有关。展开更多
基金This study was supported by a grant from the Hainan Provincial Nature Science Foundation
文摘Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BIM）, calmodulin-dependent protein kinase IIδ（CaMKIIδ） and Cyclophilin D （CypD）. Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR （qPCR） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected
文摘Objective: Emerging evidence indicates that long non-coding RNAs(lnc RNAs) are critical in carcinogenesis and progression of ovarian cancer. This study aimed to explore the functions and molecular mechanisms of plasmacytoma variant translocation I(PVT1) in ovarian cancer Methods: PVT1 and miR-214 were detected by qRT-PCR assays in ovarian cancer tissues and cells. The cell proliferation,migration, and invasion abilities were detected by cell functional experiments, respectively. Western blot assay was performed to detect epithelial-mesenchymal transition(EMT) markers. MiR-214 expression regulated by PVT1 was studied by RNA immunoprecipitation(RIP) and chromatin immunoprecipitation(Ch IP) assays.Results: The expression of PVT1 was up-regulated in ovarian cancer tissues and cell lines. Elevated PVT1 expression was associated with advanced stage and indicated poor prognosis for ovarian cancer patients. The knockdown of PVT1 impaired SKOV3 cell proliferation, migration, and invasion in vitro. The promotion of ovarian cancer progression by PVT1 involved in regulation of the epithelial-mesenchymal transition process and PVT1 interaction with EZH2 represses miR-214 expression in ovarian cancer cells.Conclusions: PVT1 plays an important role in ovarian cancer tumorigenesis, which might be as a novel diagnostic marker and therapeutic target for ovarian cancer.
文摘Objective:To explore the role of miR-214 in the progression of hepatocellular carcinoma（HCC） and its inhibitory mechanisms in depressing the signaling pathway of j3-catenin.this study was conducted.Methods:We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2.Differences between the two cell lines were compared in cell growth,proliferation,colony forming ability and cell cycles.RT-PCR method was applied for the quantification of β-catenin mRNA expression.Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets（ie.Cyclin D1,c-Myc and TCF-1）.The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression.Results:In comparison with negative（Lv-control-HepG2） and blank（HepG2） control,a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48<sup>7</sup>2h of cell culture experiments（P【0.05）.The miR-214 treatment resulted in a colony forming efficiency of（23.28±3.26）%,which was significantly lower than that of negative control[（51.31±3.97）%]（P【0.05）.According to FCM results,the experimental group,compared with control,showed a higher proportion of cells in G<sub>0</sub>/G<sub>1</sub> phase[（70.32±3.12）%]but a lower proportion in S phase[（18.42±2.90）%]（P【0.05）.The MTT assay demonstrated a significant inhibition of the proliferation and β-catenin expression of HCC cells compared with control（P【0.05）.while no significant difference was observed after HCC cells being transfected withβ-catenin overexpression plasmid（P】0.05）.By comparing to the RT-PCR and Western-blot results of control,the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression（P】0.05）.but an extremely inhibition in the protein level of β-catenin and its downstream targets Cyclin Dl,c-Myc.and TCF-1（P【0.05）.Conclusions:miR-214 functions a
文摘目的:观察8周随意跑轮运动预适应对葡聚糖硫酸钠(DSS)诱导的C57BL/6小鼠实验性溃疡性结肠炎(UC)的影响,并探讨miR-214/PTEN信号环路在其间的可能作用机制。方法:40只雄性C57BL/6小鼠随机分为4组:安静组对照组(SED-CON)、安静组造模组(SED-DSS)、运动对照组(EXE-CON)、运动造模组(EXE-DSS)。SED-CON组和SED-DSS组大鼠安静饲养8周,EXE-CON组和EXE-DSS组进行8周随意跑轮运动。随后各造模组自由饮用3.5%DSS溶液诱导小鼠UC模型,各对照组自由饮用同等量的蒸馏水。每天观察并记录体重和疾病活动指数(DAI),7天后处死小鼠,取结肠观察组织病理学变化并进行组织损伤评分,检测IL-1β、IL-6、TNF-α、miR-214、PTEN、STAT3和Akt基因表达量以及NF-κB活性。结果:与SED-DSS组比较,EXE-DSS组小鼠临床症状改善(即体重增加、DAI降低、促炎症因子表达下调、结肠组织损伤减轻)。分子生物学测定发现:与SED-DSS组比较,EXE-DSS组miR-214,Akt、STAT3、IL-6表达量以及NF-κB活性降低(P<0.05),PTEN m RNA和蛋白表达量升高(P<0.05)。结论:长期随意跑轮运动预适应能够对DSS诱导的C57BL/6小鼠实验性UC起保护效应,其机制可能与部分恢复miR-214/PTEN信号环路功能有关。
