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MAPK反义寡核苷酸诱导大鼠成纤维细胞凋亡的研究

An experimental study of antisense MAPK inducing NRK-49F apoptosis in vitro
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摘要 目的探讨MAPK反义寡核苷酸(antisenseoligodeoxynucleotide,ASO)对大鼠肾成纤维细胞凋亡的影响。方法脂质体转染法将MAPK反义寡核苷酸导入NRK-49F细胞中,Western-blotting测定细胞内MAPK蛋白的表达,DAPI染色观察细胞形态,流式细胞术检测细胞凋亡比率。结果MAPKASO降低细胞MAPK蛋白含量;且可促进细胞凋亡,转染细胞出现凋亡特征性改变,凋亡率为35.8%,与其余各组有显著差异(P<0.05)。结论MAPK反义寡核苷酸通过阻断信号转导分子MAPK诱导大鼠成纤维细胞细胞凋亡,为防治肾移植术后间质纤维化提供一定的理论依据。 [Objective] To investigate the effects of antisense MAPK on NRK-49F in vitro. [Methods] After MAPK antiserrse oligodeoxynucleotide （ASO） was transfected into NRK-49F cell line by liposome, the MAPK protein expression was assessed by Western blot, the morphological change was observed by DAPI dyeing and the apoptotic rate was detected by flow cytometry. [Results] MAPK antisense oligodeoxynucleotide could decrease protein content significantly, It also inducing the apoptosis and the apoptosis rate is 35.8% （P 〈0.05）. [Conclusion] MAPK ASO could induce apoptosis of NRK-49F through blocking the ceil signal transduction related to MAPK in vitro and can be used as a new target in the treatment of renal interstitial fibrosis after kidney transplantation.
作者 陈曦林 宫念樵 董冲 陈知水 叶启发
机构地区 华中科技大学同济医学院同济医院器官移植研究所
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2005年第17期2573-2576,共4页 China Journal of Modern Medicine
基金 国家自然基金资助项目(30300324)
关键词 丝裂素活化蛋白激酶 反义寡核苷酸 成纤维细胞 凋亡 肾纤维化 mitogen activated protein kinase antisense oligodeoxynucleotide NRK-49F, apoptosis fibrosis
分类号 R446.69 [医药卫生—诊断学] R730.45 [医药卫生—肿瘤]
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参考文献16

  • 1FINE LG, ONG AC, NORMAN JT. Mechanism of tubulo-interstitial injury in progressive renal disease [J]. Eur J Clin Invest,1993, 23(5): 259-265.
  • 2和平,刘建平,景涛,何国祥.腺病毒介导AT2R基因转染表达抑制肾间质纤维母细胞增殖[J].中国现代医学杂志,2003,13(10):16-19. 被引量：3
  • 3BADID C, VINCENT M, FOUQUE D, et al. Myofibroblast: a prognostic marker and target cell in progressive renal disease [J].Ren fail, 2001, 23: 543-549.
  • 4DINEV D, JORDAN BW, NEUFELD B, et al. Extracellular signal regulated kinaseS(ERKS) is required for the differentiation of musclecells[J]. EMBO, 2001, 2(9): 829-834.
  • 5YU W, LIAO QY, HANTASH FM, et al. Activation of extracellular signal reg~lated kinase and c-Jun NH (2) terminal kinase but not p38 mitogen activated protein kinase is required for RRR alpha tocopherylsuccinate induced apoptosis of human breast cancer cells[J]. Cancer Res, 2001, 61(17): 6569-6576.
  • 6GLENNON PE, KADDOURA S, SALE EM, et al. Depletion of mitogen activated protein kinase using an antisense oligodeoxynucleotide approach downregulates the phenylephing induced hypertrophic responses in rat cardiac myocytes [J]. Circ Res, 1996, 28: 954-961.
  • 7BRADRORD MM. A rapid and sensitive method for the quantiration of microgram quantifies of protein utilizing the pfincipIe of protein dye binding[J]. Anal Bioehem, 1976, 72: 248-254.
  • 8LAZOU A, BOGOYERITCH MA, CLERK A, etal. Regulation of mitogen activated protein kinase cascade in adult rat heart preparation invitro[J]. Circ Res, 1994, 75: 932-941.
  • 9JOOSETEN SA, VAN KOOTEN C, PAUL LC. Pathogenesis of chronic allograft rejection[J]. Transpl In4 2003, 16(3): 137-145.
  • 10EDDY AA. Molecular insights into renal interstitial fibrosis[J]. J Am Sac NephroL 1996, 7(12): 24952.

二级参考文献10

  • 1[7]Okada H, Inoue T, Kanno Y, et al. Interstitial fibroblast-like cells express renin-angiotensin system components in a fibrosing murine kidney.Am J Pathol,2002; 160(3):765～772
  • 2[8]De Paolis P, Porcellini A, Gigante B, et al. Modulation of the AT2 subtype receptor gene activation and expression by the AT1 receptor in endothelial cells. J Hypertension, 1999;17(12 Pt 2):1873～1877
  • 3[9]AbdAlla S, Lother H, Abdel-tawab AM, et al. The angiotensin Ⅱ AT2 receptor is an AT1 receptor antagonist. J Biol Chem,2001 ;276(43):39721～39726
  • 4[10]Kawano H, Do YS, Kawano Y, et al. Angiotensin Ⅱ has multiple profibrotic effects in human cardiac fibroblasts. Circulation,2000; 101 (10): 1130～1137
  • 5[1]Matsubara H. Pathophysiological role of angiotensin Ⅱ type 2 receptor in cardiovascular and renal diseases. Circ Res,1998;83:1182～1191
  • 6[2]Ma J, Nishimura H, Fogo A, et al. Accelerated fibrosis and collagen deposition develop in the renal interstitium of angiotensin type 2 receptor null mutant mice during ureteral obstruction. Kidney Int,1998;53(4): 937～944
  • 7[3]Allen AM, Zhuo J, Mendelsohn FA. Localization of angiotensin AT1 and AT2 receptors. J Am Soc Nephrol, 1999;10(Suppl 11):S23～S29
  • 8[4]Sugawara Y, Sakata Y, Minowada S, et al. Adenovirus-mediated transfer of tissue-type plasminogen activator gene to human endothelial cells. Surgery, 1997;122:91～100
  • 9[5]Matrougui K, Loufrani L, Heymes C, et al. Activation of AT2 receptors by endogenous angiotensin Ⅱ is involved in flow-induced dilation in rat resistance arteries. Hypertension, 1999;34:659～665
  • 10[6]Nozawa Y, Matsuura N, Miyake H, et al. Effects of TH-142177 on angiotensin II-induced proliferation, migration and intracellular signaling in vascular smooth muscle cells and on neointimal thickening after balloon injury. Life Science,1999; 64:2061～2070

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中国现代医学杂志
2005年 第17期

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