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组蛋白脱乙酰基酶2在血管紧张素Ⅱ致心肌细胞肥大中的表达 被引量:1

Expression of histone deacetylase 2 in hypertrophic cardiocytes induced by angiotensin Ⅱ
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摘要 目的观察血管紧张素Ⅱ(AngⅡ)刺激心肌细胞,造成心肌细胞肥大过程中组蛋白脱乙酰基酶2(histonedeacetylase2,HDAC2)的表达。方法培养原代心肌细胞,AngⅡ刺激心肌细胞造成肥大,在不同时间取细胞进行反转录聚合酶链反应(RT-PCR),观察HDAC2mRNA表达,免疫组化法检测HDAC2蛋白表达,相差镜和电镜下观察细胞形态变化。结果经AngⅡ刺激后,相差镜下可见心肌细胞面积变大;电镜下见细胞内部结构亦发生明显的改变;HDAC2mRNA水平随着AngⅡ刺激时间延长而增高;HDAC2蛋白表达亦增加。结论AngⅡ致心肌细胞肥大过程中伴有HDAC2表达增加,HDAC2有可能参与心肌细胞的肥大机制。 Objective To observe the expression of histone deacetylase 2 (HDAC2) in hypertrophiccardiocytes induced by angiotensin Ⅱ (AngⅡ). Methods The cultured cardiocytes were treated with AngⅡ toinduce hypertrophy. In different periods, the mRNA levels of HDAC2 were examined by real-time PCR method. Theprotein expressions of HDAC2 were examined by immunohistochemistry method. The morphologic changes ofcardiocytes were observed under the contrast phase microscope and electron microscope. Results The myocyteswere enlarged under the contrast phase microscope and the inner structure also changed accordingly under electronmicroscope. After stimulated by AngⅡ , the mRNA level and protein expression of HDAC2 increased in thehypertrophic cardiocytes. Conclusions The expression of HDAC2 increases in hypertrophic cardiocytes stimulatedby AngⅡ. HDAC2 may play a role in cardiocyte hypertrophy.
出处 《中国地方病学杂志》 CAS CSCD 北大核心 2005年第4期392-395,共4页 Chinese Jouranl of Endemiology
基金 黑龙江省自然科学基金资助项目(D01-51)
关键词 组蛋白脱乙酰基酶2 血管紧张素Ⅱ 心肌细胞 肥大 Histone deacetylase 2 Angiotensin Ⅱ Cardiocytes Hypertrophy
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参考文献9

  • 1周扬,翟俊民,王治伦,陈燕,吴劲.克山病病因研究进展[J].中国地方病学杂志,2004,23(5):496-498. 被引量:11
  • 2Zhang CL, McKinsey TA, Chang S, et al. Class l histone deacetylases act as signal-responsive repressors of cardiac hypertrophy[J]. Cell, 2002,110(4) :479-488.
  • 3Antos CL, McKinsey TA, Dreitz M, et al. Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors[J]. J Biol Chem, 2003,278(31 ):28930-28937.
  • 4Kramer OH, Zhu P, Ostendorff HP, et al. The histonc deacetylase inhibitor valproic acid selectively induces proteasomal degradation of HDAC2[J]. EMBO J, 2003,22(13): 3411-3420.
  • 5Kook H, Lepore J, Gitler AD, et al. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop[J]. J Clin Invest, 2003,112(6) :863-871.
  • 6Hamamori Y, Schneider MD. HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy[J]. J Clin Invest, 2003,112(6): 824-826.
  • 7Ajamian F,Salminen A,Reeben M. Selective regulation of class Ⅰand Class Ⅱ histone deacetylases expression by inhibitors of histone deacetylases in cultured mouse neural cells[J]. Neuroscience letters, 2004,365:64-68.
  • 8Tsai SC, Seto E. Regulation of histone deacetylase 2 by protein kinase CK2[J]. J Biol Chem, 2002,277(35):31826-31833.
  • 9王春梅,曹峰林,孙晶,赵立卓.肿瘤坏死因子的基因型与扩张型心肌病的相关性研究[J].中国地方病学杂志,2004,23(5):410-411. 被引量:4

二级参考文献11

  • 1Jacob CD, Lewis G d, Mcdevitl H D, et al. MHC Ⅱ associated variation in the prodDCMtion of tumor necrosis factor in mice and humans: relevance to the pathogenesis of auto -immune disease.Immunol Ros, 1991,10:156-163.
  • 2Kusske AM, Rongione A J, Reber HA. Cytokines and acute pancreatitis. Gastroenterology. 1999,118:778-796.
  • 3Marsh ET. MHC-Ⅱ nucleotiale sequentes. Tissue Antigens,2001,128:112-116.
  • 4Li YW, Peng TQ, Yang YZ, et al. High prevalence of enteroviral genomic in myocardium from cases of endemic cardiomyopathy (Keshan Disease)in China. Heart, 2000,83: 696-701.
  • 5Burke MP, Opeskin K. Fulminant heart failure due to selenium deficiency cardiomyopathy (Keshan disease). Med Sci Law,2002,42.
  • 6Liu Y, Chiba M, Inaba Y, et al. Keshan Disease-a review from the aspect of history and etiology. Nippon Eiseigaku Zasshi, 2002,56:641-648.
  • 7Peng TQ, Li YW, Yang YZ, et al. Characterization of enterovirus isolates from patients with heart muscle disease in a SeleniumDeficient Area of China. J Clin Microbiol, 2000,38:3538-3543.
  • 8Beck MA, Shi Q, Morris VC, et al. Rapid genomic evolution of a non-virulent coxsackievirus B3 in Selenium-deficient mice results in selection of identical virulent isolates. Nat Med, 1995,1:405-406.
  • 9Levander OA, Beck MA. Viral evolution as driven by host nutritional selective factors:influence of dietary oxidative stress.Food Chemistry, 1996,57:47-49.
  • 10Levander OA. The Selenium-coxsackievirus connection:Chronicle of a Collaboration. Journal of Nutrition, 2000,130: 485-488.

共引文献13

同被引文献8

  • 1Zhang CL, McKinsey TA, Chang S, et al. Class Ⅱ histone deacetylases act as signal-responsive repressors of cardiac hypertrophy[J]. Cell, 2002, 110(4):479-488.
  • 2Antos CL, McKinsey TA, Dreitz M, et al. Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors[J]. J Biol Chem, 2003, 278(31):28930-28937.
  • 3Kook H, Lepore JJ, Gitler AD, et al. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop[J]. J Clin Invest, 2003, 112(6):863-871.
  • 4Kong Y, Tannous P, Lu G, et al. Suppression of class Ⅰ and Ⅱ histone deacetylases blunts pressure-overload cardiac hypertrophy[J]. Circulation, 2006, 113(22):2579-2588.
  • 5Krmer OH, Zhu P, Ostendorff HP, et al. The histone deacetylase inhibitor valproic acid selectively induces proteasomal degradation of HDAC2[J]. EMBO J, 2003, 22(13):3411-3420.
  • 6Lee TM, Lin MS, Chang NC, et al. Inhibition of histone deacetylase on ventricular remodeling in infarcted rats[J]. Am J Physiol Heart Circ Physiol, 2007, 293(2):H968-H977.
  • 7Zeng Y, Tang CM, Yao YL, et al. Cloning and characterization of the mouse histone deacetylase-2 gene[J]. J Biol Chem, 1998, 273(44):28921-28930.
  • 8刘红利,陈燕.组蛋白乙酰化/去乙酰化及其在恶性血液病中的研究进展[J].现代临床医学生物工程学杂志,2003,9(2):146-148. 被引量:2

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