期刊文献+

大鼠非梗死区心肌Sos1/2蛋白表达的改变 被引量:2

Changes of Sos1/2 protein expression in non-infarcted myocardium in rats
原文传递
导出
摘要 目的:探讨大鼠非梗死区心肌Son of Sevenless(Sos)1/2蛋白表达的改变。方法:建立SD大鼠实验性心肌梗死(心肌梗死组)及假手术模型(假手术组),分别于术后24 h和12周处死2组大鼠各8只,获取心脏标本。应用免疫印迹法检测心肌梗死组中非梗死区心肌及假手术组心肌Sos1/2蛋白表达。结果:心肌梗死组术后12周心肌Sos1/2蛋白表达比假手术组术后24 h和术后12周及心肌梗死组术后24 h均显著增加[(0.40±0.13):(0.26±0.11):(0.24±0.08):(0.25±0.10),均P<0.05]。结论:心肌中存在Sos1/2蛋白表达。梗死后12周非梗死区心肌Sos1/2蛋白表达显著增加,提示Sos1/2蛋白表达增加参与了梗死后心脏的重塑。 Objective:To investigate the changes of Son of Sevenless(Sos)1/2 protein expression in non-infarcted myocardium in rats.Method:Experimental myocardial infarction(MI group) and sham-operation(sham group) models in SD rats were established respectively.Sos1/2 protein expression in non-infarcted myocardium in the MI group and in myocardium in the sham group was measured by Western blot respectively.Result:Sos1/2 protein expression in the non-infarcted myocardium in the MI group at 12th week after infarction [(0.40±0.13)] was significantly higher than those in the myocardium in the sham group at 24 h [(0.26±0.11)] and 12th week [(0.24±0.08)] after operation,and in the non-infarcted myocardium in the MI group at 24 h [(0.25±0.10)] after infarction respectively(All P0.05).Conclusion:Sos1/2 protein expression exists in the myocardium in rats.The increased Sos1/2 protein expression can be involved in the left ventricular remodeling after infarction.
出处 《临床心血管病杂志》 CAS CSCD 北大核心 2012年第11期865-867,共3页 Journal of Clinical Cardiology
基金 重庆市卫生局医学科学技术研究项目(No:2009-2-290 04-2-154) 重庆市科委自然科学基金计划资助项目(No:CSTC 2007BB5276)
关键词 心肌梗死 Sos1 2蛋白 鸟嘌呤核苷交换因子 心肌 myocardial infarction Sos1/2 protein guanine nucleotide exchange factor myocardium
  • 相关文献

参考文献9

  • 1KRISHNAMURTHY P, SUBRAMANIAN V, SINGH M, et al. Deficiency of betal integrins results in increased myocardial dysfunction after myocardial infarction [J]. Heat, 2006,92 : 1309 - 1315.
  • 2DING L, DONG L, CHEN X, et al. Increased expres- sion of integrin-linked kinase attenuates left ventrieular remodeling and improves cardiac function after myocardial infarction[J]. Circulation, 2009,120 : 764- 773.
  • 3HAKIM Z S, DIMICHELE L A, ROJAS M, et al. FAK regulates cardiomyocyte survival following is- chemia/reperfusion[J]. J Mol Cell Cardiol, 2009,46 241 -248.
  • 4I.AL H, VERMA S K, FOSTER D M, et al. Inte- grins and proximal signaling mechanisms in cardiovas- cular disease[J]. Front Biosci, 2009,14 : 2307- 2aa4.
  • 5周婧,李刚.羟氯喹对梗死区周边心肌共济失调毛细管扩张突变基因下游分子及凋亡的影响[J].临床心血管病杂志,2010,26(5):375-377. 被引量:2
  • 6HARSTON R K, KUPPUSWAMY D. Integrins are the necessary links to hypertrophic growth in cardiomyocytes [J]. J Signal Transduct ,2011,2011 =ID 521742,8 pages.
  • 7WHITE D E, COUTU P, SHI Y F, et al. Targeted ablation of ILK from the murine heart results in dilat- ed cardiomyopathy and spontaneous heart failure[J]. Genes Dev, 2006,20 : 2355- 2360.
  • 8PENG X, KRAUS M S, WEI H, et al. Inactivation of focal adhesion kinase in eardiomyocytes promotes eccentric cardiac hypertrophy and fibrosis in mice[J]. J Clin Invest,2006,116:217-227.
  • 9PIERRE S, BATS A S, COUMOUL X. Understand- ing SOS (Son of Sevenless)[J]. Biochem Pharmacol, 2011,82: 1049- 1056.

二级参考文献4

共引文献1

同被引文献38

  • 1Liu XL, Li G, Wang ZH, et al. Increased expression of Dock180protein in the noninfarcted myocardium in rats[J]. J Chin MedAssoc, 2013, 76(3): 164-168.
  • 2Valencik ML, Keller RS, Loftus JC, et al. A lethal perinatalcardiac phenotype resulting from altered integrin function incardiomyocytes[J]. J Card Fail, 2002, 8(4): 262-272.
  • 3Krishnamurthy P, Subramanian V, Singh M, et al. Deficiency ofβ1 integrins results in increased myocardial dysfunction aftermyocardial infarction[J]. Heart, 2006, 92(9): 1309-1315.
  • 4Ding L, Dong L, Chen X, et al. Increased expression of integrinlinkedkinase attenuates left ventricular remodeling and improvescardiac function after myocardial infarction[J]. Circulation,2009, 120(9): 764-773.
  • 5Hakim ZS, DiMichele LA, Rojas M, et al. FAK regulatescardiomyocyte survival following ischemia/reperfusion[J]. JMol Cell Cardiol, 2009, 46(2): 241-248.
  • 6Birge RB, Kalodimos C, Inagaki F, et al. Crk and CrkLadaptor proteins: networks for physiological and pathologicalsignaling[J]. Cell Commun Signal, 2009, 7: 13.
  • 7Feller SM. Crk family adaptors-signalling complex formation andbiological roles[J]. Oncogene, 2001, 20(40): 6348-6371.
  • 8Zhang X, Li G, Zhang L, et al. C3G overexpression promotes the survival of rat-derived H9C2 cardiomyocytes by p-ERK1/2[J].Cell Biol Int, 2013, 37(10): 1106-1113.
  • 9Gu R, Bai J, Ling L, et al. Increased expression of integrin-linkedkinase improves cardiac function and decreases mortality indilated cardiomyopathy model of rats[J]. PLoS One, 2012, 7(2):e31279.
  • 10Harston RK, Kuppuswamy D. Integrins are the necessary links tohypertrophic growth in cardiomyocytes[J]. J Signal Transduct,2011, 2011: 521742.

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部