目的:探讨先天性甲状腺功能减退症(congenital hypothyroidism,CH)大鼠海马中Ca^(2+)/钙调蛋白依赖性蛋白激酶Ⅳ(Ca^(2+)/calmodulin-dependent protein kinaseⅣ,CAMK4)及早期生长反应蛋白3(early growth response protein 3,EGR3)信...目的:探讨先天性甲状腺功能减退症(congenital hypothyroidism,CH)大鼠海马中Ca^(2+)/钙调蛋白依赖性蛋白激酶Ⅳ(Ca^(2+)/calmodulin-dependent protein kinaseⅣ,CAMK4)及早期生长反应蛋白3(early growth response protein 3,EGR3)信号轴对神经元树突发育的影响。方法:1日龄、7日龄及21日龄SD大鼠制备CH模型,分为CH组与对照组。采用转录组测序、q-PCR、Western blot分别检测CAMK4与EGR3的表达情况,细胞免疫荧光观察神经元树突生长情况。结果:(1)对照组海马组织CAMK4及EGR3的蛋白表达呈时间依赖性上升,CH组的表达则显著低于对照组(P <0.05);(2)原代海马神经元中敲降CAMK4后,EGR3的表达相应降低,同时海马神经元树突平均长度较对照组减小;(3)CH原代海马神经元给予三碘甲腺原氨酸(3,5,3′-triiodothyronine,T3)刺激后,CAMK4的蛋白表达水平呈时间依赖性上升。结论:甲状腺激素缺乏会导致大鼠海马CAMK4及EGR3表达降低,从而抑制神经元树突的发育,表明CAMK4-EGR3信号轴可能在CH大鼠海马神经发育异常中发挥重要作用。展开更多
Objective： Hepatocellular carcinoma （HCC） is still one of the most common death-related malignancies worldwide. Because the way onset and progression are hidden most, HCC diagnoses are made at an advanced stage, wh...Objective： Hepatocellular carcinoma （HCC） is still one of the most common death-related malignancies worldwide. Because the way onset and progression are hidden most, HCC diagnoses are made at an advanced stage, when they are unsuitable for surgical resection. MicroRNAs are a class of small non-coding RNAs, participating in many aspects of cancers. In this study, we tried to establish the role of micreRNA-718 （miR-718） in the malignant phenotype of HCC cells and its possible role in HCC diagnosis. Methods： Here we first used a methylthiazolyldiphenyl- tetrazolium bromide （MTT） assay, Transwell migration and invasion assays, and colony formation assay to evaluate the impact of miR-718 on the malignant phenotypes of HCC cells. Then, we used bioinformatic methods to predict the target gene of miR-718 and used green fluorescence protein （GFP） reporter assay, Western blot, and quantitative real-time polymerase chain reaction （qRT-PCR） to validate the regulation relationship. Finally, we determined the role of the target gene in the HCC phenotype. Results： We found that the expression of miR-718 was significantly reduced in various HCC cell lines and HCC tissues. Re-expression of miR-718 significantly reduced the cellular viability and colony formation ability as well as inhibited the migration and invasion abilities of HCC cell lines. Early growth response protein 3 （EGR3） is a direct target of miR-718 and is negatively regulated by miR-718. EGR3 could increase the via- bility and proliferation of HCC cells, and promot the migration and invasion of HCC cells. Conclusions： miR-718 acts as a tumor suppressive microRNA in HCC via regulating the expression of EGR3, which may provide a new diagnostic 07） found that overexpreget for HCC.展开更多
文摘目的:探讨先天性甲状腺功能减退症(congenital hypothyroidism,CH)大鼠海马中Ca^(2+)/钙调蛋白依赖性蛋白激酶Ⅳ(Ca^(2+)/calmodulin-dependent protein kinaseⅣ,CAMK4)及早期生长反应蛋白3(early growth response protein 3,EGR3)信号轴对神经元树突发育的影响。方法:1日龄、7日龄及21日龄SD大鼠制备CH模型,分为CH组与对照组。采用转录组测序、q-PCR、Western blot分别检测CAMK4与EGR3的表达情况,细胞免疫荧光观察神经元树突生长情况。结果:(1)对照组海马组织CAMK4及EGR3的蛋白表达呈时间依赖性上升,CH组的表达则显著低于对照组(P <0.05);(2)原代海马神经元中敲降CAMK4后,EGR3的表达相应降低,同时海马神经元树突平均长度较对照组减小;(3)CH原代海马神经元给予三碘甲腺原氨酸(3,5,3′-triiodothyronine,T3)刺激后,CAMK4的蛋白表达水平呈时间依赖性上升。结论:甲状腺激素缺乏会导致大鼠海马CAMK4及EGR3表达降低,从而抑制神经元树突的发育,表明CAMK4-EGR3信号轴可能在CH大鼠海马神经发育异常中发挥重要作用。
基金Project supported by the Science and Technology Project of Higher Education of Shandong Province(No.J12LK07),China
文摘Objective： Hepatocellular carcinoma （HCC） is still one of the most common death-related malignancies worldwide. Because the way onset and progression are hidden most, HCC diagnoses are made at an advanced stage, when they are unsuitable for surgical resection. MicroRNAs are a class of small non-coding RNAs, participating in many aspects of cancers. In this study, we tried to establish the role of micreRNA-718 （miR-718） in the malignant phenotype of HCC cells and its possible role in HCC diagnosis. Methods： Here we first used a methylthiazolyldiphenyl- tetrazolium bromide （MTT） assay, Transwell migration and invasion assays, and colony formation assay to evaluate the impact of miR-718 on the malignant phenotypes of HCC cells. Then, we used bioinformatic methods to predict the target gene of miR-718 and used green fluorescence protein （GFP） reporter assay, Western blot, and quantitative real-time polymerase chain reaction （qRT-PCR） to validate the regulation relationship. Finally, we determined the role of the target gene in the HCC phenotype. Results： We found that the expression of miR-718 was significantly reduced in various HCC cell lines and HCC tissues. Re-expression of miR-718 significantly reduced the cellular viability and colony formation ability as well as inhibited the migration and invasion abilities of HCC cell lines. Early growth response protein 3 （EGR3） is a direct target of miR-718 and is negatively regulated by miR-718. EGR3 could increase the via- bility and proliferation of HCC cells, and promot the migration and invasion of HCC cells. Conclusions： miR-718 acts as a tumor suppressive microRNA in HCC via regulating the expression of EGR3, which may provide a new diagnostic 07） found that overexpreget for HCC.
