目的探讨γ干扰素(interferon-gamma,INF-γ)、微小RNA-29a(microRNA-29a,miR-29a)、原癌基因PIM-1(proto-oncogene PIM-1,PIM-1)标志物在结核性胸膜炎合并胸腔积液中的表达水平变化及其与临床特征的关系。方法选取2021年5月—2023年6...目的探讨γ干扰素(interferon-gamma,INF-γ)、微小RNA-29a(microRNA-29a,miR-29a)、原癌基因PIM-1(proto-oncogene PIM-1,PIM-1)标志物在结核性胸膜炎合并胸腔积液中的表达水平变化及其与临床特征的关系。方法选取2021年5月—2023年6月在某医院就诊的107例结核性胸膜炎患者为研究对象,按照诊断结果分为结核性胸膜炎合并胸腔积液组(n=69)和单纯结核性胸膜炎组(n=38)。对比两组INF-γ、miR-29a、PIM-1表达水平差异,Spearman相关系数分析INF-γ、miR-29a、PIM-1表达水平与结核性胸膜炎合并胸腔积液的相关性;受试者操作特征(receiver operator characteristic,ROC)曲线分析INF-γ、miR-29a、PIM-1及其联合检测对结核性胸膜炎合并胸腔积液的预测效能,计量资料数据比较分析采用t检验,计数资料的比较采用χ^(2)检验。结果与单纯结核性胸膜炎组相比,结核性胸膜炎合并积液组的INF-γ(t=-5.440,P<0.001)、miR-29a(t=-3.561,P=0.001)、PIM-1(t=-3.232,P=0.002)均升高;Spearman相关系数分析显示,INF-γ、miR-29a、PIM-1表达水平与结核性胸膜炎合并胸腔积液呈正相关(r=0.443,P<0.001;r=0.332,P<0.001;r=0.291,P=0.002);ROC曲线显示,INF-γ、miR-29a、PIM-1单独及联合检测预测结核性胸膜炎合并胸腔积液的曲线下面积(area under the curve,AUC)分别为0.764、0.701、0.663和0.838,与INF-γ、miR-29a、PIM-1单独检测相比,联合检测对结核性胸膜炎合并胸腔积液具有较高的诊断效能(Z=1.983、2.168、2.859,P=0.047、0.030、0.004)。结论结核性胸膜炎合并胸腔积液患者INF-γ、miR-29a、PIM-1表达水平均表现为特异性的上调,这种联合检测对预测结核性胸膜炎患者是否合并胸腔积液具有良好的预测效能,值得临床推广应用。展开更多
BACKGROUND At present,the incidence of diabetic nephropathy is increasing year by year,and there are many studies on the pathogenesis of diabetic nephropathy,but it is still not completely clear.The final pathological...BACKGROUND At present,the incidence of diabetic nephropathy is increasing year by year,and there are many studies on the pathogenesis of diabetic nephropathy,but it is still not completely clear.The final pathological result of diabetic nephropathy is mainly glomerular cell fibrosis,and the roles of micro-RNA(miRNA)-29 and DNA methyl transferase(DNMTs)in cell fibrosis have been confirmed in other studies,but there is a lack of relevant research in the kidney at present.AIM To study the potential involvement of miRNA-29a-3p in fibrosis related to diabetic kidney disease(DKD).METHODS The expression of miR-29a-3p,DNMT3A/3B,fibrosis-related molecules,Wnt3a,β-catenin,Janus kinase 2,and signal transducer and activator of transcription 3 was assessed in SV40MES13 cells and diabetic mice using quantitative real-time PCR and western blotting.Furthermore,the expression changes of fibrosis-related molecules were further analyzed using immunofluorescence and immunohistochemical blotting.The renal pathological changes of DKD in each group were also studied using hematoxylin-eosin and periodate-Schiff reaction staining.RESULTS In both the in vivo and in vitro experiments,it was observed that high glucose induction significantly decreased miR-29a-3p expression.As a result of this downregulation,DKD-related fibrosis was found to be promoted,as confirmed by elevated expression levels ofα-smooth muscle actin,collagen type I,and fibronectin.MiR-29a-3p targets the 3’non-coding regions of DNMT3A and DNMT3B and inhibits their expression.Inhibition of DNMT3A and DNMT3B can reverse the effect of miR-29a-3p downregulation on DKD-related fibrosis.CONCLUSION MiR-29a-3p can regulate Wnt/β-catenin and Janus kinase/signal transducer and activator of transcription signal pathways by regulating and inhibiting the expression of DNMT3A/3B and thus participate in the inhibition of DKD-related fibrosis.展开更多
文摘目的探讨γ干扰素(interferon-gamma,INF-γ)、微小RNA-29a(microRNA-29a,miR-29a)、原癌基因PIM-1(proto-oncogene PIM-1,PIM-1)标志物在结核性胸膜炎合并胸腔积液中的表达水平变化及其与临床特征的关系。方法选取2021年5月—2023年6月在某医院就诊的107例结核性胸膜炎患者为研究对象,按照诊断结果分为结核性胸膜炎合并胸腔积液组(n=69)和单纯结核性胸膜炎组(n=38)。对比两组INF-γ、miR-29a、PIM-1表达水平差异,Spearman相关系数分析INF-γ、miR-29a、PIM-1表达水平与结核性胸膜炎合并胸腔积液的相关性;受试者操作特征(receiver operator characteristic,ROC)曲线分析INF-γ、miR-29a、PIM-1及其联合检测对结核性胸膜炎合并胸腔积液的预测效能,计量资料数据比较分析采用t检验,计数资料的比较采用χ^(2)检验。结果与单纯结核性胸膜炎组相比,结核性胸膜炎合并积液组的INF-γ(t=-5.440,P<0.001)、miR-29a(t=-3.561,P=0.001)、PIM-1(t=-3.232,P=0.002)均升高;Spearman相关系数分析显示,INF-γ、miR-29a、PIM-1表达水平与结核性胸膜炎合并胸腔积液呈正相关(r=0.443,P<0.001;r=0.332,P<0.001;r=0.291,P=0.002);ROC曲线显示,INF-γ、miR-29a、PIM-1单独及联合检测预测结核性胸膜炎合并胸腔积液的曲线下面积(area under the curve,AUC)分别为0.764、0.701、0.663和0.838,与INF-γ、miR-29a、PIM-1单独检测相比,联合检测对结核性胸膜炎合并胸腔积液具有较高的诊断效能(Z=1.983、2.168、2.859,P=0.047、0.030、0.004)。结论结核性胸膜炎合并胸腔积液患者INF-γ、miR-29a、PIM-1表达水平均表现为特异性的上调,这种联合检测对预测结核性胸膜炎患者是否合并胸腔积液具有良好的预测效能,值得临床推广应用。
基金Supported by the Chongqing Basic Research and Frontier Exploration Project,No.cstc2018jcyjAX0834.
文摘BACKGROUND At present,the incidence of diabetic nephropathy is increasing year by year,and there are many studies on the pathogenesis of diabetic nephropathy,but it is still not completely clear.The final pathological result of diabetic nephropathy is mainly glomerular cell fibrosis,and the roles of micro-RNA(miRNA)-29 and DNA methyl transferase(DNMTs)in cell fibrosis have been confirmed in other studies,but there is a lack of relevant research in the kidney at present.AIM To study the potential involvement of miRNA-29a-3p in fibrosis related to diabetic kidney disease(DKD).METHODS The expression of miR-29a-3p,DNMT3A/3B,fibrosis-related molecules,Wnt3a,β-catenin,Janus kinase 2,and signal transducer and activator of transcription 3 was assessed in SV40MES13 cells and diabetic mice using quantitative real-time PCR and western blotting.Furthermore,the expression changes of fibrosis-related molecules were further analyzed using immunofluorescence and immunohistochemical blotting.The renal pathological changes of DKD in each group were also studied using hematoxylin-eosin and periodate-Schiff reaction staining.RESULTS In both the in vivo and in vitro experiments,it was observed that high glucose induction significantly decreased miR-29a-3p expression.As a result of this downregulation,DKD-related fibrosis was found to be promoted,as confirmed by elevated expression levels ofα-smooth muscle actin,collagen type I,and fibronectin.MiR-29a-3p targets the 3’non-coding regions of DNMT3A and DNMT3B and inhibits their expression.Inhibition of DNMT3A and DNMT3B can reverse the effect of miR-29a-3p downregulation on DKD-related fibrosis.CONCLUSION MiR-29a-3p can regulate Wnt/β-catenin and Janus kinase/signal transducer and activator of transcription signal pathways by regulating and inhibiting the expression of DNMT3A/3B and thus participate in the inhibition of DKD-related fibrosis.
