目的:探讨CCN3对牙周膜成纤维细胞(periodontal ligament fibroblasts,PDLFs)增殖和凋亡的作用及可能的机制。方法:构建重组载体pc DNA.3.1-CCN3并转染人PDLFs过表达CCN3,转染CCN3 si RNA,抑制其表达量。转染Fra-1 si RNA到抑制CCN3的PD...目的:探讨CCN3对牙周膜成纤维细胞(periodontal ligament fibroblasts,PDLFs)增殖和凋亡的作用及可能的机制。方法:构建重组载体pc DNA.3.1-CCN3并转染人PDLFs过表达CCN3,转染CCN3 si RNA,抑制其表达量。转染Fra-1 si RNA到抑制CCN3的PDLFs,同时抑制CCN3和Fra-1的表达量。应用实时荧光定量PCR(q RT-PCR)检测CCN3、Fra-1 m RNA表达水平,Western印迹法检测CCN3、Fra-1和Bcl-2蛋白表达量。MTT和Brd U实验分别检测PDLFs的生长活力和增殖能力。试剂盒方法检测caspase-3的活性。采用SPSS20.0软件包对数据进行统计学分析。结果:转染pc DNA.3.1-CCN3的实验中,CCN3 m RNA(P<0.05)和蛋白(P<0.05)表达量显著上升。转染CCN3 si RNA的实验中,CCN3 m RNA(P<0.05)和蛋白(P<0.05)表达量显著下降。CCN3表达量被抑制后,PDLFs的增殖能力(P<0.05)和生长活力(P<0.05)显著上升,caspase-3活性(P<0.05)和Bcl-2蛋白表达量(P<0.05)分别降低和升高。然而,CCN3过表达时作用相反。CCN3过表达或抑制可分别显著降低(P<0.05)或促进(P<0.01)Fra-1的表达量。另外,同时抑制CCN3和Fra-1,可促进PDLFs的凋亡(P<0.01)且抑制其增殖能力(P<0.05)。结论:抑制CCN3可通过上调Fra-1的表达,促进PDLFs的增殖能力并抑制其凋亡。展开更多
Postpartum psychosis is a severe psychiatric condition which affects 1-2 of every 1000 mothers shortly after childbirth. Whilst there is convincing evidence that the condition is precipitated by a complex combination ...Postpartum psychosis is a severe psychiatric condition which affects 1-2 of every 1000 mothers shortly after childbirth. Whilst there is convincing evidence that the condition is precipitated by a complex combination of biological and environmental factors, as yet the pathophysiological mechanisms remain extremely poorly defined. Here, I critically review approaches that have been, or are being, employed to identify and characterise such mechanisms; I also review a recent animal model approach, and describe a novel biological risk model that it suggests. Clarification of biological risk mechanisms underlying disorder risk should permit the identification of relevant predictive biomarkers which will ensure that "at risk" subjects receive prompt clinical intervention if required.展开更多
文摘目的探讨中晚期孕妇血清NOV/CCN3水平变化,并分析其与妊娠期糖尿病(gestational diabetes mellitus,GDM)及妊娠结局的关系。方法根据口服葡萄糖耐量实验(oral glucose tolerance test,OGTT)结果,将252例妊娠女性分为GDM组与对照组。根据妊娠前体质量指数水平及妊娠结局情况将GDM组进行分组。收集所有研究对象临床资料,比较组间一般资料、生化指标及NOV/CCN3水平的差异。结果GDM组血清NOV/CCN3水平高于对照组(P<0.001)。Spearman相关分析结果表明血清NOV/CCN3与妊娠前体质量、妊娠前体质量指数、胰岛素抵抗指数、总胆固醇呈正相关,与胰岛素敏感指数呈负相关(P<0.05)。logistic回归分析结果表明,NOV/CCN3是GDM发生的独立危险因素[OR=1.097,95%CI(1.020~1.179),P=0.013],且是GDM患者发生不良妊娠结局的独立危险因素[OR=1.032,95%CI(1.020~1.045),P<0.001],ROC分析结果显示曲线下面积(area under the curve,AUC)分别为0.840、0.784(P<0.05)。结论中晚期孕妇血清NOV/CCN3水平与肥胖、胰岛素抵抗及糖脂代谢相关,参与GDM发生发展,为评估中晚期孕妇发生GDM及GDM患者妊娠结局提供新的思路。
文摘目的:探讨CCN3对牙周膜成纤维细胞(periodontal ligament fibroblasts,PDLFs)增殖和凋亡的作用及可能的机制。方法:构建重组载体pc DNA.3.1-CCN3并转染人PDLFs过表达CCN3,转染CCN3 si RNA,抑制其表达量。转染Fra-1 si RNA到抑制CCN3的PDLFs,同时抑制CCN3和Fra-1的表达量。应用实时荧光定量PCR(q RT-PCR)检测CCN3、Fra-1 m RNA表达水平,Western印迹法检测CCN3、Fra-1和Bcl-2蛋白表达量。MTT和Brd U实验分别检测PDLFs的生长活力和增殖能力。试剂盒方法检测caspase-3的活性。采用SPSS20.0软件包对数据进行统计学分析。结果:转染pc DNA.3.1-CCN3的实验中,CCN3 m RNA(P<0.05)和蛋白(P<0.05)表达量显著上升。转染CCN3 si RNA的实验中,CCN3 m RNA(P<0.05)和蛋白(P<0.05)表达量显著下降。CCN3表达量被抑制后,PDLFs的增殖能力(P<0.05)和生长活力(P<0.05)显著上升,caspase-3活性(P<0.05)和Bcl-2蛋白表达量(P<0.05)分别降低和升高。然而,CCN3过表达时作用相反。CCN3过表达或抑制可分别显著降低(P<0.05)或促进(P<0.01)Fra-1的表达量。另外,同时抑制CCN3和Fra-1,可促进PDLFs的凋亡(P<0.01)且抑制其增殖能力(P<0.05)。结论:抑制CCN3可通过上调Fra-1的表达,促进PDLFs的增殖能力并抑制其凋亡。
基金Supported by Medical Research Council Centre for Neuro-psychiatric Genetics and Genomics,No.MR/L010305/1
文摘Postpartum psychosis is a severe psychiatric condition which affects 1-2 of every 1000 mothers shortly after childbirth. Whilst there is convincing evidence that the condition is precipitated by a complex combination of biological and environmental factors, as yet the pathophysiological mechanisms remain extremely poorly defined. Here, I critically review approaches that have been, or are being, employed to identify and characterise such mechanisms; I also review a recent animal model approach, and describe a novel biological risk model that it suggests. Clarification of biological risk mechanisms underlying disorder risk should permit the identification of relevant predictive biomarkers which will ensure that "at risk" subjects receive prompt clinical intervention if required.
