Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whe...Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.展开更多
目的研究缺血性脑卒中患者血清差异基因的筛选及生物信息学。方法以2023年3月-2024年3月在新疆医科大学第二附属医院神经内科确诊的80例缺血性脑卒中患者为病例组,选择同期80例健康体检者为对照组。分别挑选两组各10例受试者的外周血清...目的研究缺血性脑卒中患者血清差异基因的筛选及生物信息学。方法以2023年3月-2024年3月在新疆医科大学第二附属医院神经内科确诊的80例缺血性脑卒中患者为病例组,选择同期80例健康体检者为对照组。分别挑选两组各10例受试者的外周血清采用芯片差异性基因鉴定法筛选缺血性脑卒中差异表达的长链非编码RNA(lncRNA),并采用KEGG通路富集和基因本体论(GO)分析鉴定差异表达基因发挥的生物学功能。挑选2个上调和2个下调的lncR-NAs,在两组患者外周血中采用实时荧光定量PCR(qRT-PCR)法检测表达量,采用受试者工作特征曲线(Receiver operating characteristic,ROC)计算差异性表达lncRNAs诊断缺血性脑卒中的曲线下面积(Area under the curve,AUC)。结果共检测到34个高表达和16个低表达的lncR-NAs。KEGG通道分析显示,差异表达的lncRNAs涉及肿瘤坏死因子(TNF)信号通路、类风湿性关节炎、细胞因子与细胞因子受体相互作用,病毒蛋白与细胞因子和细胞因子受体的相互作用、癌症的转录失调、沙门氏菌感染、白细胞介素(IL)-17信号通路、趋化因子信号通路。GO分析显示,差异表达的lncRNAs涉及白细胞黏附调控、细胞黏附调节、白细胞与其他细胞黏附、细胞趋化性、T细胞活化、骨髓细胞分化、止血和凝血。qRT-PCR检测显示,与对照组比较,病例组患者A1BG-AS1和BRWD1-AS2表达量升高,BVES-AS1和C10ORF71-AS1表达量降低,差异有统计学意义(P<0.05)。ROC分析显示,A1BG-AS1、BRWD1-AS2、BVES-AS1和C10ORF71-AS1表达量诊断缺血性脑卒中的AUC分别为0.803、0.856、0.897和0.798(P<0.001)。结论缺血性脑卒中患者外周血中A1BG-AS1、BRWD1-AS2、BVES-AS1和C10ORF71-AS1基因差异性表达,可以辅助缺血性脑卒中的疾病诊断。展开更多
基金This work was supported by the Hunan Provincial Education Department General Project Research Fund(No.20C1412)the Hunan Graduate Scientific Research Innovation Project(No.CX2018B474)the National Famous Elderly Chinese Medicine Experts Xinyu Chen Inheritance Workshop Construction Project(No.[2022]75).
文摘Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.
文摘目的研究缺血性脑卒中患者血清差异基因的筛选及生物信息学。方法以2023年3月-2024年3月在新疆医科大学第二附属医院神经内科确诊的80例缺血性脑卒中患者为病例组,选择同期80例健康体检者为对照组。分别挑选两组各10例受试者的外周血清采用芯片差异性基因鉴定法筛选缺血性脑卒中差异表达的长链非编码RNA(lncRNA),并采用KEGG通路富集和基因本体论(GO)分析鉴定差异表达基因发挥的生物学功能。挑选2个上调和2个下调的lncR-NAs,在两组患者外周血中采用实时荧光定量PCR(qRT-PCR)法检测表达量,采用受试者工作特征曲线(Receiver operating characteristic,ROC)计算差异性表达lncRNAs诊断缺血性脑卒中的曲线下面积(Area under the curve,AUC)。结果共检测到34个高表达和16个低表达的lncR-NAs。KEGG通道分析显示,差异表达的lncRNAs涉及肿瘤坏死因子(TNF)信号通路、类风湿性关节炎、细胞因子与细胞因子受体相互作用,病毒蛋白与细胞因子和细胞因子受体的相互作用、癌症的转录失调、沙门氏菌感染、白细胞介素(IL)-17信号通路、趋化因子信号通路。GO分析显示,差异表达的lncRNAs涉及白细胞黏附调控、细胞黏附调节、白细胞与其他细胞黏附、细胞趋化性、T细胞活化、骨髓细胞分化、止血和凝血。qRT-PCR检测显示,与对照组比较,病例组患者A1BG-AS1和BRWD1-AS2表达量升高,BVES-AS1和C10ORF71-AS1表达量降低,差异有统计学意义(P<0.05)。ROC分析显示,A1BG-AS1、BRWD1-AS2、BVES-AS1和C10ORF71-AS1表达量诊断缺血性脑卒中的AUC分别为0.803、0.856、0.897和0.798(P<0.001)。结论缺血性脑卒中患者外周血中A1BG-AS1、BRWD1-AS2、BVES-AS1和C10ORF71-AS1基因差异性表达,可以辅助缺血性脑卒中的疾病诊断。
