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钙网蛋白及基质金属蛋白酶在扩张型心肌病发病机制中的作用 被引量:1

Effects of calreticulin and matrix metalloproteinases in the pathogenesis of dilated cardiomyopathy
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摘要 目的 探讨扩张型心肌病与钙网蛋白(Calreticulin)、基质金属蛋白酶(MMPs)家族成员MMP-2和MMP-9之间的关系,为扩张型心肌病的预防和治疗提供理论论据.方法 试验分两组:扩张型心肌病组和对照组.分别收集14例扩张型心肌病患者及14例对照组全血及临床资料(年龄,性别,左房、右房、左室、右室舒张末期内径及左室射血分数等),提取血浆,通过蛋白免疫印迹法(western blotting)测定血浆钙网蛋白的表达水平,通过明胶酶谱法(Gelatin-PAGE)检测各标本血浆中MMP-2和MMP-9活性.结果 ①扩张型心肌病组与对照组比较,两组间左房、左室舒张末期内径、左室射血分数和MMP-9活性的差异有统计学意义.②在扩张型心肌病组中,MMP-9活性与左室射血分数呈负相关(r=-0.590,P<0.05),与左室舒张末径呈正相关(非正态分布等级相关:r=0.396,P<0.05),但与左房、右房、右室舒张末径和室间隔厚度均无相关关系.对照组中,MMP-9与左房、右房、左室、右室舒张末径和室间隔厚度均无相关关系.③两组比较,MMP-2活性差异无统计学意义,与左房、右房、左室、右室舒张末径,左室射血分数和室间隔厚度之间均无相关关系.④钙网蛋白在扩张型心肌病组的表达升高,但与对照组相比,两者间的表达水平差异无统计学意义(P>0.05).结论 ①MMP-9在扩张型心肌病患者左室重构中起重要作用,MMP-9的活性可作为评估心功能情况的参考指标之一.②钙网蛋白在扩张型心肌病病理过程中未直接参与其疾病发展,但未排除通过其他途径作用于该病理过程. Objective To explore effects of calreticulin and matrix metalloproteinases in the pathogenesis of dilated cardiomyopathy. Methods The objects of study were divided into two groups: dilated eardiomyopathy group and control group. The persons without heart disease and pulmonary disease were selected in the control group. Both groups plasma and clinical information were collected. The expression of CRT in both groups were detected by the western blotting. The enzymatic activity of MMP-2 and MMP-9 in both groups were detected by the Gelatin-PAGE. Results (1)The enzymatic activity of MMP-9, left ventricular ejection fraction (LVEF) and the left ventricular end-diastolic diameter (LVDd) in DCM patients had significant difference compared to the control group (P〈0.05). (2)The activity of MMP-9 had relationship with the left ventricular end-diastolic diameter (LVDd) and left ventricular ejection fraction(LVEF) compared to the control group(r=0.396, P〈0.05 ). (3)On the contrary, there was no relationship between the activity of MMP-9 and the fight ventricnlar diameter (RV), left atrium (LA), right atrium (RA), intact ventricular septum (IVS). The activity of MMP-2 had no defference between two groups. MMP-2 also had no relationship with patients' LA, RA, RV, LVEF, LVDd and IVS. (4)There was no difference in the expression of CRT between two groups. Conclusion (1)The plasma MMP-9 had probably played important role in ECM degradation and ventricle remodeling in DCM patient. (2)Calreticulin was not directly involved in the pathogenesis development of DCM, but not exclusive role through other channels in the pathological process.
出处 《中国心血管病研究》 CAS 2011年第11期810-814,共5页 Chinese Journal of Cardiovascular Research
基金 国家自然科学基金项目 (30700326) 2009年汕头大学医学院基础与临床科研基金资助
关键词 扩张型心肌病 钙网蛋白 基质金属蛋白酶 Dilated cardiomyopathy Calreticulin Matrix metalloproteinases.
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参考文献18

  • 1Bielecka-dabrowa A, Wierzbicka M, Dabrowa M, et al. New methods in laboratory diagnostics of dilated cardiomyopathy. Car- diol J, 2008,15 : 388-395.
  • 2Ashwath ML, Dearmond SJ, Culclasure T. Prion associated dilat- ed cardiomyopathy. Arch Intern Med, 2005,165 : 338-340.
  • 3Visse R, Nagase H. Matrix metalloproteinases and tissue in- hibitors of metalloproteinases structure function and biochemistry. Circ Res, 2003,92 : 827-839.
  • 4Wu M, Li YG. The expressions of CD40-CD40L and activities of matrix metalloproteinase in atherosclerotic rats. Molecular and Cellular Biochemistry, 2006,282 : 141-146.
  • 5Vinet L, Rouet-Benzineb P, Marniquet X, et al. Chronic doxy- cycline exposure accelerates left ventrice!ar hypertrophy and pro- gression to heart failure in mice after thoracic aorta constriction. Am j Physiol Heart Circ Physic!, 2008,295 : H352-360.
  • 6Zhang JS, Nie L, Razavian M, et al. Molecular imaging of acti- vated matrix metalloproteinases in vascular remodeling. Circula-tion, 2008,118 .. 1953-1960.
  • 7Wu Min, Mesaeli N, Durston M, et al. Differential expression and activity of MMP-2 and MMP-9 in calreticulin deficient ceils. Matrix Biolo, 2007,26 : 463-472.
  • 8Kleiner DE, Stetler-Steverson WG. Quantitative zymogTaphy: de- tection of picogram quantities of gelatinases. Anal Biochem,1994,218:235.
  • 9张修伟,杨英珍,王齐冰,陈瑞珍,何梅先,童步高,蔡乃绳,李高平,沈学东,陈灏珠.扩张型心肌病102例临床分析[J].中华心血管病杂志,2001,29(1):56-57. 被引量:31
  • 10秦继迅.蛋白质印迹技术在生物医学中的应用方法[J].遵义科技,2010(1):52-54. 被引量:2

二级参考文献32

  • 1陈浩,江力勤,刘加芳,张春燕,刘晓杰.核素心肌灌注断层显像鉴别诊断缺血性和扩张型心肌病[J].浙江临床医学,2005,7(3):317-318. 被引量:3
  • 2[1]Diez J, Lavindes C, Mayor G, et al. Incrcased serum concentrations of procollagen peptides in essential hypertension relation to cardiac alterations [ J ]. Circulation, 1995,91:1450 - 1456
  • 3[2]Lundgren Eullberg D, Rubin K, et al. In vitro studies on adult cardiac myoeytes: Attachment and biosynthesis of collagen type Ⅳand laminin[J].J Cell Physiol,1998,136:43-53
  • 4[4]Klappacher G, Franzen P, Haab D, et al. Measuring extracelluar matrix tumover in the serum of patients with idiopathic or ischemic dilated cardiomyopathy and impact on diagnosis and prognosis [J]. Am J Cardiol,1995,75:913 - 918
  • 5[5]Pitt B. "Escape"of aldosterone sterone production in patients with left ventricular dysfunction treated with an angiotensin converting enzyme inhibitor; implications for therapy[J]. Cardiovasc Drugs Ther, 1995,9:145 - 149
  • 6[6]Briua CG, Zhou GP, Rupp H, et al. Role of angiotensin Ⅱ and pro- Staglandin E2 in regulating cardiac fiberoblast collagen tullagen tumover[J]. Am J Cardiol, 1995,76: 8D- 13D
  • 7[7]Faiez Z, Brigitte D, Francois A. Treatment of congestive heart failure interfering the aldosterone- cardiac extracellular matrix relationship [ J ]. Hypertension,2001,38:1227 - 1232
  • 8[1]Richardson P,Mckenna W,Bristow M,et al.Report of the 1994 World Health Organization/International Society and Federation of cardiology task force on the definition and classification of cardiomyopathies.Circulation,1996,93:841-842.
  • 9[3]Same N,Doughg R.Epidemiology of heart failure and ventricular dysfunction.Lancet,1998,352(Supple):S3-S7.
  • 10[4]Gill JS O,Ward DE.Increased QT dispersion related to syncope in patients with idopathic tachycardia.Br Heart,1994,71 (Supple):S147-S149.

共引文献97

同被引文献20

  • 1Houle D,Govindaraju DR,Omholt S. Phenomics:the next challenge[J].Nature Reviews Genetics,2010.855-866.
  • 2Whitelaw E,Martin DI. Retrotransposons as epigenetic mediators of phenotypic variation in mammals[J].Nature Genetics,2001.361-365.
  • 3Hershberger RE,Morales A,Siegfried JD. Clinical and genetic issues in dilated cardiomyopathy:a review for genetics professionals[J].Genetics in Medicine,2010.655-667.
  • 4Bagnall RD,Ingles J,Semsarian C. Molecular diagnostics of cardio-myopathies:the future is here[J].Circ Cardiovasc Genet,2011.103-104.
  • 5Hershberger RE,Siegfried JD. State of the Art Review.Update 2011:clinical and genetic issues in familial dilated cardiomyopathy[J].Journal of the American College of Cardiology,2011.1641-1649.
  • 6Hershberger RE,Parks SB,Kushner JD. Coding sequence mutations identified in MYH7,TNNT2,SCN5A,CSRP3,LBD3,and TCAP from 313 patients with familial or idiopathic dilated cardiomyopathy[J].Clin Translational Science,2008.21-26.
  • 7Hershberger RE,Norton N,Morales A. Coding sequence rare variants identified in MYBPC3,MYH6,TPM1,TNNC1,and TNNI3 from 312 patients with familial or idiopathic dilated cardio-myopathy[J].Circ Cardiovasc Genet,2010.155-161.
  • 8Villard E,Perret C,Gary F. A genome-wide association study identifies two loci associated with heart failure due to dilated cardio-myopathy[J].European Heart Journal,2011.1065-1076.
  • 9Norton N,Li D,Reider MJ. Genome-wide studies of copy number variation and exome sequencing identify rare variants inBAG3as a cause of dilated cardiomyopathy[J].American Journal of Human Genetics,2011.273-282.
  • 10Cooper LT Jr,Onuma OK,Sagar S. Genomic and proteomic analysis of myocarditis and dilated cardiomyopathy[J].Heart Fail Clin,2010.75-85.

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