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.
