Over-expression of MORC2 attenuates steatosis in L02 hepatocytes by down-regulating p53

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Over-expression of MORC2 attenuates steatosis in L02 hepatocytes by down-regulating p53

更新时间：2026-01-09

- Over-expression of MORC2 attenuates steatosis in L02 hepatocytes by down-regulating p53
- Journal of Army Medical University Vol. 37, Issue 10, Pages: 962-967(2015)
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  CLC： R394-33;R394.2;R575.5
- Published：2015
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王涛,雷增杰,王斌,李青,王春华,刘琴,魏艳玲,王军,陈东风.过表达MORC2通过下调p53含量抑制L02肝细胞脂肪变性[J].陆军军医大学学报(原第三军医大学学报),2015,37(10):962-967.

　Wang Tao,Lei Zengjie,Wang Bin,Li Qing,Wang Chunhua,Liu Qin,Wei Yanling,Wang Jun,Chen Dongfeng.Over-expression of MORC2 attenuates steatosis in L02 hepatocytes by down-regulating p53[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(10):962-967.
王涛,雷增杰,王斌,李青,王春华,刘琴,魏艳玲,王军,陈东风.过表达MORC2通过下调p53含量抑制L02肝细胞脂肪变性[J].陆军军医大学学报(原第三军医大学学报),2015,37(10):962-967. DOI：

　Wang Tao,Lei Zengjie,Wang Bin,Li Qing,Wang Chunhua,Liu Qin,Wei Yanling,Wang Jun,Chen Dongfeng.Over-expression of MORC2 attenuates steatosis in L02 hepatocytes by down-regulating p53[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(10):962-967. DOI：

摘要

目的研究过表达MORC2对人L02肝细胞脂肪变性程度的影响及可能机制。方法利用慢病毒转染技术在L02肝细胞中过表达MORC2，qRT-PCR及Western blot鉴定过表达效果后，对L02肝细胞进行脂肪变性诱导，测定细胞甘油三酯（triglyceride，TG）含量并比较过表达前后L02肝细胞的脂肪蓄积程度；利用芯片技术对过表达MORC2前后的基因表达谱进行检测与Pathway分析，筛选过表达MORC2时发生变化的通路并选择对脂代谢有调控作用的p53进行研究； Western blot检测在L02肝细胞脂肪变性诱导时过表达MORC2对p53蛋白含量的影响；在过表达MORC2的基础上对L02肝细胞过表达p53，qRT-PCR及Western blot鉴定p53过表达效果后，通过TG测定观察过表达p53对过表达MORC2改变的L02肝细胞脂肪蓄积程度产生的影响。结果 qRT-PCR及Western blot证明过表达MORC2成功；过表达MORC2的L02肝细胞在脂肪变性诱导后TG含量较MORC2正常表达的L02肝细胞明显降低（P0.01）；基因表达谱芯片及Pathway分析显示脂代谢调控相关的p53通路在过表达MORC2后发生变化；Western blot显示过表达MORC2后，L02肝细胞中p53蛋白水平在脂肪变性诱导前后均降低；qRT-PCR及Western blot验证p53过表达成功，且过表达p53可部分解除MORC2对L02肝细胞脂肪变性的缓解作用。结论过表达MORC2可通过下调p53从而缓解肝细胞脂肪变性。

Abstract

Objective To investigate the effect of microrchidia family CW-type zinc finger 2 (MORC2) over-expression on steatosis of immortalized hepatocyte line L02 and explore the potential mechanism. Methods MORC2 was over-expressed in L02 hepatocytes by lentivirus transfection

and then examined by qRT-PCR and Western blotting. Intracellular triglyceride (TG) was measured to evaluate cellular steatosis. A microarray chip was adopted to analyze related signaling pathways in the MORC2 over-expression process. Over-expression of p53 in the MORC2-over-expressed L02 hepatocytes was confirmed by qRT-PCR and Western blotting

and the effect of p53 over-expression on lipid accumulation was observed by measuring TG. Results Both qRT-PCR and Western blot data validated that MORC2 was over-expressed in the transfected L02 hepatocytes. Steatosis was significantly alleviated by MORC2 over-expression (P0.01). The microarray chip data revealed that lipometabolism-related p53 pathway was changed after MORC2 over-expression. Western blot results demonstrated that p53 protein was down-regulated after MORC2 over-expression. Moreover

over-expression of p53 partially increased steatosis in the MORC2-over-expressed L02 hepatocytes. Conclusion MORC2 attenuates steatosis of L02 hepatocytes partially by down-regulating p53 expression.

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