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JAK1/STAT3参与的eNOS基因转染对心肌梗死后血管形成的影响 被引量:2

Effects of JAK/STAT3-involved eNOS gene transfer on angiogenesis after myocardial infarction
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摘要 目的探讨JAK1/STAT3参与的eNOS基因转染对心肌梗死(MI)后血管形成的影响。方法采用Wistar大鼠,建立基因转染和心肌梗死模型,观察eNOS基因转染对信号通道蛋白表达、心脏功能和血管形成的影响。结果与对照组比较,eNOS基因转染后,eNOS表达明显增加、JAK1/STAT3表达明显增加、NO生成明显提高[(0.42±0.04)nmol/mgvs.(0.18±0.02)nmol/mg](P<0.01)、MI面积减少、血管形成明显增加,MI后7d心脏功能明显改善。结论 eNOS基因转染后MI面积明显减少、心脏功能明显改善,血管形成明显增加;eNOS基因对MI后血管形成的作用可能与增加JAK1/STAT3的表达有关。 Objective To study the effects of JAK/STAT3-involved endothelial nitric oxide synthase(eNOS) gene transfer on the angiogenesis after myocardial infarction(MI).Methods Human eNOS gene in an adenovirus vector was delivered locally into male Wistar rats heart 4 days prior to MI induced by left anterior descending coronary artery ligation.Neovascularization was identified immunohistochemically.Expression of JAK1/STAT3 was detected by Western blot.ResultsCompared to the controls,eNOS gene transfer significantly increased the expressions of eNOS and JAK1/STAT3 and production of NO,stimulated the angiogenesis,reduced myocardial infarct size and improved cardiac contractility on the 7th day after MI.Conclusion eNOS/NO system provides cardiac protection on MI injury through stimulates angiogenesis and action of JAK1/STAT3 signaling.
出处 《江苏医药》 CAS CSCD 北大核心 2010年第19期2303-2305,F0003,共4页 Jiangsu Medical Journal
关键词 心肌梗死 ENOS基因 JAK1/STAT3 Myocardial infarction Endothelial nitric oxide synthase gene (eNOS gene) JAK1/STAT3
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  • 1Fukuda S, Kaga S, Zhan L, et al. Resveratrol ameliorates myocardial damage by inducing vascular endothelial growth factor-angiogenesis and tyrosine kinase receptor Flk-1 [J]. Cell Bioehem Biophys, 2006,44 (1) : 43-49.
  • 2Uemura R,Xu M, Ahmad N, et al. Bone marrow stem cells prevent left ventrieular remodeling of ischemic heart through paracrine signaling[J]. Circ Res, 2006,98(11) : 1414-1421.
  • 3Scherrer-Crosbie M, Ullrich R, Bloch KD, et al. Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice[J ]. Circulation, 2001,104 ( 11 ) : 1286-1291.
  • 4Yamakuchi M,Greer JJ,Cameron SJ, et al. HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size [J]. Circ Res, 2005, 96 ( 11 ): 1185- 1192.
  • 5Takahashi K,Fukushima S, Yamahara K, et al. Modulated inflammation by injection of high-mobility group box 1 recovers post-infarction chronically failing heart [J]. Circulation, 2008,118(14 Suppl) : 106-114.
  • 6Bujak M, Dobaczewshi M, Chatila K, et al. Interleukin-1 receptor type Ⅰ signaling critically regulates infarct healing and cardiac remodeling[J]. Am J Pathol, 2008,173 ( 1 ): 57-67.
  • 7Ockaili R, Natarajan R, Salloum F,et al. HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation [J]. Am J Physiol Heart Circ Physiol, 2005,289 (2) : 542-548.
  • 8Lu L, Zhang JQ, Ramires FJ,et al. Molecular and cellular events at the site of myocardial infarction: from the perspective of rebuilding myocardial tissue[J]. Biochem Biophys Res Commun, 2004,320 (3) : 907-913.
  • 9Zhang MX, Zhao X,Wang ZG, et al. Constitutive activation of signal transducer and activator of transcription 3 regulates expression of vascular endothelial growth factor in human meningioma differentiation [J]. J Cancer Res Clin Oncol, 2010,136 (7) : 981-988.
  • 10Alas S, Bonavida B. Inhibition of constitutive STAT3 activity sensitizes resistant non-Hodgkin's lymphoma and multiple myeloma to chemotherapeutic drug-mediated apoptosis[J]. Clin Cancer Res, 2003,9 (1) : 316-326.

同被引文献12

  • 1Hansson GK. Inflammation, atherosclerosis, and coronary artery disease[J]. N Engl J Med,2005,352(16) .. 1685-1695.
  • 2Harismendy O, Notani D, Song X, et al. 9p21 DNA variants associated with coronary artery disease impair interferon-γ signalling response[J]. Nature, 2011,470 (7333) : 264-268.
  • 3Booteov MR, Bauskin AR, Valenzuela SM, et al. MIC-1, a novel macrophage inhibitory eytokine, is a divergent member of the TGF-beta superfamily[J]. Proc Natl Acad Sci USA, 1997,94(21) : 11514-11519.
  • 4Kempf T, Eden M, Strelau J, et al. The transforming growth factor-beta superfamily member growth-differentiation factor- 15 protects the heart from ischemia/reperfusion injury[J]. Circ Res, 2006,98(3) .. 351-360.
  • 5Xu J, Kimball TR, Lorenz JN, et al. GDF15/MIC-1 functions as a protective and antihypertrophic factor released from the myocardium in association with SMAD protein activation[J]. Circ Res, 2006,98(3) : 342-350.
  • 6Kempf T, Bjorklund E, Olofsson S, et al. Growth- differentiation factor-15 improves risk stratification in ST- segment elevation myocardial infarction [ J ]. Eur Heart J, 2007,28 (23) : 2858-2865.
  • 7Khan SQ, Ng K, Dhillon O, et al. Growth differentiation factor-15 as a prognostic marker in patients with acute myocardial infarction [J]. Eur Heart J, 2009, 30 ( 9 ) .. 1057- 1065.
  • 8Wang X, Yang X, Sun K, et al. The haplotype of the growth- differentiation factor 15 gene is associated with left ventricular hypertrophy in human essential hypertension[J]. Clin Sci(Lond), 2009,118 (2) : 137-145.
  • 9Chen Z, Xie F, Ma G, et al. Study of the association between growth differentiation factor 15 gene polymorphism and coronary artery disease in a Chinese population[J]. Mol Biol Rep, 2011,38 (8) : 5085-5091.
  • 10Gensini GG. A more meaningful scoring system for deter- mining the severity of coronary heart disease [J]. Am J Cardiol, 1983,51 (3) : 606.

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