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实时荧光定量PCR检测转基因阿尔茨海默病小鼠脑组织中miRNAs的差异表达 被引量:8

Real-time PCR for detecting differential expressions of microRNAs in the brain of a transgenic mouse model of Alzheimer's disease
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摘要 目的通过实时荧光定量PCR方法检测APPswe/PS△E9双转基因小鼠和对照小鼠脑组织中miRNA-135a-5p、miRNA-135a-2-3p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p的表达。方法选取6月龄大小的APPswe/PS△E9双转基因小鼠为实验组,同月龄同种系的野生型小鼠C57为对照组,分别提取其脑组织总miRNA,应用实时荧光定量PCR方法检测两组小鼠脑组织中miRNA-135a-5p、miRNA-135a-2-3p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p的表达。结果上述5种miRNAs在实验组与对照组小鼠中的相对表达量分别为0.73±0.27、1.08±0.58,2.47±6.15、1.65±0.67,0.72±0.14、1.31±0.73,0.57±0.34、1.06±0.35,0.63±0.26、1.02±0.18。其中有统计学意义的是miRNA-135a-5p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p(P≤0.05)。结论 miRNA-135a-5p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p在APPswe/PS△E9双转基因小鼠中有差异表达,可能在阿尔茨海默病的发病过程中起着重要作用。 Objective To detect the expression of miRNA-135a-5p, miRNA-135a-2-3p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p in the brain tissue of the APPswe/PS △ E9 double transgenic mouse model of Alzhaimer's disease using real-time PCR. Methods Six-month-old APPswe/PS △ E9 double transgenic mice and wild-type C57 mice of the same species were examined for the expressions of miRNA-135a-5p, miRNA-135a-2-3p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p in the brain tissue using real-time PCR. Results The relative expression levels of the 5 miRNAs in the transgenic versus the wild-type mice were 0.73±0.27 vs 1.08±0.58, 2.47±6.15 vs 1.65±0.67, 0.72±0.14 vs 1.31±0.73, 0.57±0.34 vs 1.06±0.35, and 0.63+0.26 vs 1.02±0.18, respectively,showing sign/ficance differences in the expressions of miRNA-135a-Sp, miRNA-298-Sp, miRNA-466b-3p, and miR-669f-3p between the two groups (P〈0.05). Conclusion miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p are expressed differentially in APPswe/PS △ E9 double transgenic mice, suggesting their important roles in the pathogenesis of Alzheimer disease.
出处 《南方医科大学学报》 CAS CSCD 北大核心 2013年第2期262-266,共5页 Journal of Southern Medical University
基金 湖南省科技厅社会发展支撑计划课题(009SK3175 2012SK3218)
关键词 阿尔茨海默病 转基因阿尔茨海默病小鼠 miRNA 实时荧光定量PCR Alzheimer disease transgenic mice microRNA real-time polymerase chain reaction
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参考文献18

  • 1Roshan R,Ghosh T,Scaria V. MicroRNAs:novel therapeutic targets in neurodegenerative diseases[J].Drug Discovery Today,2009,(23-24):1123-1129.
  • 2Junn E,Mouradian MM. MicroRNAs in neurodegenerative diseases and their therapeutic potential[J].Pharmacology and Therapeutics,2012,(02):142-150.
  • 3丁宇,田密,刘建锋,邓炎尧,李维,奉夏露,侯德仁.APPswe/PS△E9双转基因小鼠脑组织miRNA的表达[J].南方医科大学学报,2012,32(9):1280-1283. 被引量:5
  • 4Sathya M,Premkumar P,Karthick C. BACE1 in alzheimer's disease[J].Clinica Chimica Acta,2012,(0):171-178.
  • 5Zong Y,Wang H,Dong W. miR-29c regulates BACE1 protein expression[J].Brain Research,2011.108-115.
  • 6Fang M,Wang J,Zhang X. The miR-124 regulates the expression of BACE1/β-secretase correlated with cell death in Alzheimer's disease[J].Toxicology Letters,2012,(01):94-105.
  • 7Zhu HC,Wang LM,Wang M. MicroRNA-195 downregulates Alzheimer's disease amyloid-β production by targeting BACE1[J].Brain Research Bulletin,2012,(06):596-601.
  • 8Delay C,Mandemakers W,Hebert SS. MicroRNAs in Alzheimer's disease[J].Neurobiology of Disease,2012,(02):285-290.
  • 9Delay C,Calon F,Mathews P. Alzheimer-specific variants in the 3'UTR of Amyloid precursor protein affect microRNA function[J].MOLECULAR NEURODEGENERATION,2011.70.
  • 10Wang WX,Rajeev BW,Stromberg AJ. The expression of microRNA miR-107 decreases early in Alzheimer's disease and may accelerate disease progression through regulation of beta-site amyloid precursor protein-cleaving enzyme 1[J].The Journal of Neuroscience,2008,(05):1213-1223.doi:10.1523/JNEUROSCI.5065-07.2008.

二级参考文献15

  • 1Christensen M, Schratt GM. MicroRNA involvement in developmental and functional aspects of the nervous system and neurological diseases[J]. Neurosci Lett, 2009, 466(2): 55-62.
  • 2Junn E, Mouradian MM. MicroRNAs in neurodegenerative diseases and their therapeutic potential [J]. Pharmacol Ther, 2012, 133(2):142-50.
  • 3Satoh J. MieroRNAs and their therapeutic potential for human diseases: aberrant microRNA expression in Alzheimer's disease brains[J]. J Pharmacol Sci, 2010, 114(3): 269-75.
  • 4Provost P. MicroRNAs as a molecular basis for mental retardation, Alzheimer's and priori diseases[J]. Brain Res, 2010, 1338: 58-66.
  • 5Maes OC, Chertkow HM, Wang E, et al. MicroRNA: Implications for Alzheimer disease and other human CNS disorders [J]. Curr Genomics, 2009, 10(3): 154-68.
  • 6Peter T, Wang WX, Rajeev BW, MicroRNAs(miRNAs) in neurodegenerative diseases[J]. Brain Pathol, 2008, 18(1): 130-8.
  • 7Zhou ZD, Chan CH, Ma QH, et al. The roles of amyloid precursor protein(APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimeri disease[J]. Cell Adhesion Migration, 2011, 5 (4): 280-92.
  • 8Bettens K, Brouwers N, Engelborhs S, et al. APP and BACE1 miRNA genetic variability has no major role in risk for Alzheimer disease[J]. Hum Mutat, 2009, 30(8): 1207-13.
  • 9Hebert SS, Horre K, Nicolai L, et al. Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer's disease correlates with increased BACE1/beta-secretase expression[J]. Proc Natl Acad Sci USA, 2008, 105(17): 6415-20.
  • 10Nelson PT, Wang WX. MiR-107 is reduced in Alzheimer's disease brain neocortex: validation study[J]. J Alzheimers Dis, 2010, 21(1): 75-9.

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同被引文献66

  • 1吴越.阿尔茨海默病发生机制的microRNA水平研究进展[J].中国老年学杂志,2014,34(12):3506-3508. 被引量:5
  • 2Van Hoesen GW, Augustinack JC, Dierking J, et al. The parahippocampal gyms in Alzheimer's disease.Clinical and preclinical neuroanatomical correlates[J]. Ann N Y Acad Sci, 2000, 911: 254-74.
  • 3Wang HY, D'Andrea MR, Nagele RG. Cerebellar diffuse amyloid plaques are derived from dendritic Abeta42 accumulations in Purkinje cells[J]. Neurobiol Aging, 2002, 23(2): 213-23.
  • 4Sepulveda-Falla D, Matschke J, Bernreuther C, et al. Deposition of hyperphosphorylated tau in cerebellum of PSI E280A Alzheimer's disease[J]. Brain Pathol, 2011, 21(4): 452-63.
  • 5Mavroudis IA, Fotiou DF, Adipepe LF, et al. Morphological changes of the human purkinje cells and deposition of neuritic plaques and neurofibrillary tangles on the cerebellar cortex of Alzheimer's disease[J]. Am J Alzheimers Dis Other Demen, 2010, 25(7): 585-91.
  • 6Lomoio S, L6pez-Gonzilez I, Aso E, et al. Cerebellar amyloid-13 plaques: disturbed cortical circuitry in AI]PP/PS1 transgenic mice as a model of familial Alzheimer's disease [J]. J Alzheimers Dis, 2012, 31(2): 285-300.
  • 7Aso E, Lomoio S, L6pez-Gonzllez I, et al. Amyloid generation and dysfunctional immunoproteasome activation with disease progression in animal model of familial Alzheimer's disease [J]. Brain Pathol, 2012, 22(5): 636-53.
  • 8Yakushev I, Landvogt C, Buchholz HG, et al. Choice of reference area in studies of Alzheimer's disease using positron emission tomography with fluorodeoxyglucose-F18 [J]. Psychiatry Res, 2008, 164(2): 143-53.
  • 9Delay C, Mandemakers W, Hebert SS. MicroRNAs in alzheimer's diseas[J]. Neuorbio Dis, 2012, 46(2): 485-90.
  • 10Satoh J. Molecular network of microRNA targets in Alzheimer's disease brains[J]. Exp Neurol, 2012, 235(2): 436-46.

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