Neuron-derived clone 77 (Nur77) is a member of the NR4A subfamily that plays critical roles in apoptosis, survival, proliferation, autophagy, angiogenesis, inflammatory responses, DNA repair, glycolipid metabolism and...Neuron-derived clone 77 (Nur77) is a member of the NR4A subfamily that plays critical roles in apoptosis, survival, proliferation, autophagy, angiogenesis, inflammatory responses, DNA repair, glycolipid metabolism and energy consumption. The deregulation of Nur77 signalling often relates to various serious diseases, including cancer and non-cancer diseases. A systematic review is necessary for the better understanding of Nur77 in clinical treatment. In this article, we comprehensively conclude the lipid regulation function and expression of Nur77, and its role in COPD. Finally, we prospect that development of drugs and clinical biochemical investigations targeting of Nur77 has considerable potential within healthcare.展开更多
目的研究肝大部分切除术(PHx)后核受体Nur77调控肝细胞进入增殖周期的分子机制。方法在Nur77基因敲除型(knockout,KO)和野生型对照组中构建PHx诱导的小鼠肝再生模型,用组织学染色、生化、定量PCR以及蛋白免疫印迹(western-blot,WB)等方...目的研究肝大部分切除术(PHx)后核受体Nur77调控肝细胞进入增殖周期的分子机制。方法在Nur77基因敲除型(knockout,KO)和野生型对照组中构建PHx诱导的小鼠肝再生模型,用组织学染色、生化、定量PCR以及蛋白免疫印迹(western-blot,WB)等方法检测再生肝组织的形态学、血清学改变,以及相应基因的表达情况。结果PHx术后多个时间点KO组肝脏均出现组织坏死,KO组术后48 h、72 h的血清ALT均高于WT组(466.3±202.4 vs 72.0±58.8,486.2±156.3 vs 63.0±0.3,P<0.05)。凋亡细胞特异性染色示KO组术后3 h和48 h的凋亡细胞计数高于对照组(38.7±9.6 vs 2.8±0.2,87.3±19.4 vs 8.4±3.1,P<0.05)。PHx术后早期KO组肝脏的凋亡基因caspase-8与剪切caspase-3蛋白均上调。结论Nur77缺失诱导肝再生早期肝细胞凋亡。展开更多
文摘Neuron-derived clone 77 (Nur77) is a member of the NR4A subfamily that plays critical roles in apoptosis, survival, proliferation, autophagy, angiogenesis, inflammatory responses, DNA repair, glycolipid metabolism and energy consumption. The deregulation of Nur77 signalling often relates to various serious diseases, including cancer and non-cancer diseases. A systematic review is necessary for the better understanding of Nur77 in clinical treatment. In this article, we comprehensively conclude the lipid regulation function and expression of Nur77, and its role in COPD. Finally, we prospect that development of drugs and clinical biochemical investigations targeting of Nur77 has considerable potential within healthcare.
文摘目的研究肝大部分切除术(PHx)后核受体Nur77调控肝细胞进入增殖周期的分子机制。方法在Nur77基因敲除型(knockout,KO)和野生型对照组中构建PHx诱导的小鼠肝再生模型,用组织学染色、生化、定量PCR以及蛋白免疫印迹(western-blot,WB)等方法检测再生肝组织的形态学、血清学改变,以及相应基因的表达情况。结果PHx术后多个时间点KO组肝脏均出现组织坏死,KO组术后48 h、72 h的血清ALT均高于WT组(466.3±202.4 vs 72.0±58.8,486.2±156.3 vs 63.0±0.3,P<0.05)。凋亡细胞特异性染色示KO组术后3 h和48 h的凋亡细胞计数高于对照组(38.7±9.6 vs 2.8±0.2,87.3±19.4 vs 8.4±3.1,P<0.05)。PHx术后早期KO组肝脏的凋亡基因caspase-8与剪切caspase-3蛋白均上调。结论Nur77缺失诱导肝再生早期肝细胞凋亡。
