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人肝热缺血安全时限的基因芯片分析 被引量:3

Analysis of safe limit of human hepatic warm ischemic time by microarray
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摘要 目的 探讨人肝不同缺血时限细胞凋亡相关基因的多基因表达模式和差异表达 ,为掌握肝缺血安全时限提供科学依据。方法 应用基因芯片表达谱技术观测正常人肝组织与肝缺血 15min(组一 )、30min(组二 )及肝缺血 15min与 30min(组三 )相比较细胞基因表达状况 ,对 2 0 0点特异性凋亡相关基因差异表达进行分析比较。结果 肝缺血 0~ 15min ,凋亡相关基因的表达基本处于低表达或正常表达水平 ,表达明显上调的的差异表达基因主要为调节细胞内环境稳定的基因 ;而至肝缺血 30min ,各种维系细胞和细胞器内环境稳定的调控基因表达水平明显下降 ,多种促凋亡发生的相关基因、诱导凋亡发生的核转录因子则明显活化、表达上调。结论 一般而言 ,人肝一次热缺血时限以尽量不超过 Objective To investigate different patterns of expression of multiple genes in human ischemic liver to provide evidence about safe limit of human hepatic ischemia. Methods The responses of cells to hepatic ischemia and hypoxia after hepatic ischemia for 15 and 30 min were analyzed by cDNA microarray representing 4000 different genes containing 200 apoptotic correlative genes. Results During the period of hepatic ischemia for 0-15 min, there were lower or normal expression levels of apoptotic correlative genes and the maintenance hemostatic genes were expressed significantly higher. However, the expression levels of maintenance hemostatic genes were down-regulated and the expression of many apoptotic correlative genes and nuclear transcription factors were activated and up-regulated. Conclusions The safe limit of human hepatic warm ischemic time is generally less than 30 min.
出处 《中华肝胆外科杂志》 CAS CSCD 2004年第6期366-368,共3页 Chinese Journal of Hepatobiliary Surgery
基金 本课题受国家自然科学基金 (项目编号 :3 0 170 92 8) 全军医学科研十五计划课题 (项目编号 :0 1MA0 40 )资助
关键词 肝缺血 安全时限 凋亡相关基因 肝热缺血 基因芯片 内环境 调控基因表达 细胞器 促凋亡 差异表达 Hepatic ischemia Safe time Gene expression Gene microarray
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  • 1Izban KF, Ergin M, Martinez RL, et al. Expression of the tumor necrosis factor receptor-associated factors (TRAFs) 1and 2 is a characteristic feature of Hodgkin and Reed-Sternberg cells. Mod Pathol, 2000, 13:1324-1331.
  • 2Onishi I, Yoshioka K, Yamamoto K, et al. Activation of c-Jun N-terminal kinase during ischemia and reperfusion in mouse liver. FEBS Lett, 1997, 420: 201-204.
  • 3Sasaki H, Tanaka N, Nakagawa K, et al. Induction of apoptosis during the early phase of reperfusion after rat liver ischemia. Acta Med Okayama, 1997, 51: 305-312.
  • 4Miyazaki K, Yoshida H, Sasaki M, et al. Caspase-independent cell death and mitochondrial disruptions observed in the apaf1-deficient cells. J Biochem (Tokyo), 2001,129 : 963-969.
  • 5Neuman MG. Apoptosis in diseases of the liver. Crit Rev Clin Lab Sci, 2001, 38:109-166.
  • 6Hoeflich KP, Yeh WC, Yao Z, et al. Mediation of TNF receptor-associated factor effector functions by apoptosis signal-regulating kinase-1 (ASK1). Oncogene, 1999, 18:5814-5820.
  • 7Cao Z, Xiong J, Taleuchi M, et al. TRAF6 is a signal transducer for interleukin-1. Nature, 1996,383: 443-446.

同被引文献88

  • 1Chen YY,Zhao YG,Zhang T,et al.Preparation and identification of monoclonal antibodies against human programmed cell death 10 (PD-CD10).Beijing Da Xue Xue Bao,2006,38(6):586-591.
  • 2Ma X,Zhao H,Shan J,et al.PDCD10 interacts with Ste20-related kinase MST4 to promote cell growth and transformation via modulation of the ERK pathway.Mol Biol Cell,2007,18(6):1965-1978.
  • 3Bergametti F,Denier C,Labange P,et al.Mutations within the programmed cell death 10 gene cause cerebral cavernous malformations.Am J Hum Cenet,2005,76(1):42-51.
  • 4Busch CR,Heath DD,Hubberstey A.Sensitive genetic biomarkers for determining apoptosis in the brown bullhead.Gene,2004,329:1-10.
  • 5Xu Y,Kulkosky J,Acheampoag E,et al.HIV-1-mediated apoptosis of neuronal cells:Proximal molecular mechanisms of HIV-1-induced encephalopathy.Proc Natl Acad Sci USA,2004,101 (18):7070-7075.
  • 6Felbor U,Sure U,Grimm T,et al.Genetics of cerebral cavernous angioma.Zentralhl Neurochir,2006,67(3):110-116.
  • 7Wang QK.Update on the Molecular Genetics of Vascular Anomalies.Lymphat Res Biol,2005,3(4):226-233.
  • 8Tanriover G,Boylan AJ,Diluna ML,et al.PDCD10,the gene mutated in cerebral cavernons malformation 3,is expressed in the neurovascular unit.Neurosurgery,2008,62(4):930-938.
  • 9Stahl S,Gaetzner S,Voss K,et al.Novel CCM1,CCM2,and CCM3 mutation in patients with cerebral cavernous malformations:in-frame deletion in CCM2 prevents formation of a CCM1/CCM2/ CCM3 protein complex.Hum Mutat,2008,29(5):709-717.
  • 10Hilder TL,Malone MH,Bencharit S,et al.Proteomic identification of the cerebral cavernous malformation signaling complex.J Proteome Res,2007,6(11):4343-4355.

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