期刊文献+

先天性心脏病并肺动脉高压患者肺组织eNOS、MMP-1、TIMP-1的表达变化及意义 被引量:2

Change and significance of eNOS,MMP-1 and TIMP-1 in lung tissue of patients with CHD and pulmonary hypertension
下载PDF
导出
摘要 目的观察先天性心脏病(CHD)并发肺动脉高压(PH)患者肺组织中内皮型一氧化氮合酶(eNOS)与基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶组织抑制因子-1(TIMP-1)的表达变化,并探讨其意义。方法光镜下观察60例CHD患者肺小动脉形态,按照Heath-Edwards PH分级法分组,CHD无PH患者14例为对照组,CHD合并PHⅠ、Ⅱ、Ⅲ级46例为观察组。采用RT-PCR技术检测患者肺组织中eNOS mRNA、MMP-1 mRNA、TIMP-1 mRNA。结果 MMP-1 mRNA、TIMP-1 mRNA、TIMP-1 mRNA/MMP-1 mRNA在观察组的表达高于对照组(P均<0.01),eNOS mRNA则低于观察组(P<0.01)。MMP-1 mRNA与TIMP-1 mRNA的表达呈正相关(r=0.879,P<0.01);MMP-1 mRNA、TIMP-1 mRNA、TIMP-1 mRNA/MMP-1 mRNA与PH分级呈正相关(r分别为0.858、0.802、0.315,P均<0.05),eNOS mRNA与PH分级呈负相关(r=-0.714,P<0.01);TIMP-1 mRNA、MMP-1 mRNA、TIMP-1mRNA/MMP-1 mRNA与eNOS mRNA呈负相关(r分别为-0.607、-0.642、-0.777,P均<0.01)。结论 CHD合并PH患者肺组织中eNOS、MMP-1、TIMP-1表达失调,参与肺血管重构及PH形成过程。 Objective To study the change and significance of eNOS,MMP-1 and TIMP-1 expression in lung tissue of patients with congenital heart disease(CHD)and pulmonary hypertension(PH).Methods CHD patients were divided into different groups according to Heath-Edwards pulmonary vessel pathologic grading: control group(non-PH)14 cases,observation group(PHⅠ,PHⅡ,PH Ⅲ)46 cases.The eNOS mRNA,MMP-1 mRNA and TIMP-1 mRNA were detected by RT-PCR in the lung tissue of these patients.Results The levels of MMP-1 mRNA,TIMP-1 mRNA and TIMP-1 mRNA/MMP-1 mRNA were raised in observation group with control group(P0.01),eNOS mRNA was decreased in observation group with control group(P0.01).There was significant positive correlation between the MMP-1 mRNA and TIMP-1 mRNA(r=0.879,P0.01).There were significant positive correlation between MMP-1 mRNA,TIMP-1 mRNA,TIMP-1 mRNA/MMP-1 mRNA and the grade of PH(r were 0.858,0.802 and 0.315,all P0.05).There was significanthy negative correlation between the eNOS mRNA and the grade of PH(r=-0.714,P0.01).There were singificantly negative correlation between TIMP-1 mRNA,MMP-1 mRNA,TIMP-1 mRNA/MMP-1 mRNA and eNOS mRNA(r were-0.607,-0.642 and-0.777,all P0.01).Conclusion eNOS and MMP-1/TIMP-1 imbalance may contribute to pulmonary vascular remodeling in CHD with PH.
出处 《山东医药》 CAS 北大核心 2011年第18期10-11,共2页 Shandong Medical Journal
基金 广西壮族自治区自然科学基金资助项目(0640087)
关键词 肺动脉高压 先天性心脏病 一氧化氮合酶 基质金属蛋白酶 基质金属蛋白酶组织抑制因子 pulmonary hypertension congenital heart disease nitric oxide synthase matrix metalloproteinases tissue inhibitor of matrix metalloproteinases
  • 相关文献

参考文献6

  • 1Mandegar M,Fung YC,Huang W,et al.Cellular and molecular mechanisms of pulmonary vascular remodeling:role in the development of pulmonary hypertension[J].Microvasc Res,2004,68(2):75-103. 被引量:1
  • 2Farber HW,Loscalzo J.Pulmonary Arterial Hypertension[J].N Engl J Med,2004,351(16):1655-1665. 被引量:1
  • 3王伟,王玉林.肺动脉高压发病机制研究进展[J].实用儿科临床杂志,2008,23(13):1036-1038. 被引量:6
  • 4陈树宝主编..小儿心脏病学进展[M].北京:科学出版社,2005:580.
  • 5Brown DJ,Lin B,Chwa M,et al.Elements of the nitric oxide pathway can degrade TIMP-1 and increase gelatinase activity[J].Mol Vis,2004,16(10):281-288. 被引量:1
  • 6Junbao D,Hui Y,Bing W,et al.Effect of L-arginine on collagen of high flow-induced pulmonary arterial remodeling[J].Circ J,2005,69(5):603-608. 被引量:1

二级参考文献19

  • 1Lane KB, Machado RD, Pauciulo MW, et al. Heterozygous germline mutations in BMPR2 encoding a TGF -beta recepor,cause familial primary pulmonary hypertension. The international PPH consortium [ J ]. Nat Genet,2000,26( 1 ) :81 -84. 被引量:1
  • 2Aldred MA, Vijayakrlshnan J, James V, et al. BMPR2 gene rearrangements account for a significant proportion of mutations in familial and idiopathic pulmonary arterial hypertension [ J ]. Hum Murat, 2006,27 (2) :212 -213. 被引量:1
  • 3Song Y,Jones JE,Beppu H,et al. Increased susceptibility to pulmonary hypertension in heterozygous BMPR2 - mutant mice [ J ]. Circulal ,n, 2005,112(4) :553 -562. 被引量:1
  • 4Teichert - Kuliszewska K, Kutryk M J, Kuliszewski MA, et al. Bone morphogenetic protein receptor -2 signaling promotes pulmonary arterial endothelial cell survival : Implications for loss - of - function mutations in the pathogenesis of pulmonary hypertension [ J ]. Circ Res ,2006 ,98 (2) : 209 -217. 被引量:1
  • 5Atkinson C, Stewart S, Upton PD,et al. Primary pulmonary hypertension is associated with reduced pulmonary vascular expression of type Ⅱ bone morphogenetic protein receptor [ J ]. Circulation, 2002,105 ( 14 ) : 1672 - 1678. 被引量:1
  • 6Kitaura H, Uozumi N ,Tohmi M ,et al. Roles of nitric oxide as a vasodilatot in neurovascular coupling of mouse somatosensory cortex[ J]. Neurosci Res,2007,59(2) :160 - 171. 被引量:1
  • 7Fisher KA, Serlin DM, Wilson KC ,et al. Sarcoidosis -associated pulmonary hypertension:Outcome with long -term epoprostenol treatment[ J ]. Chest ,2006,130(5 ) : 1481 - 1488. 被引量:1
  • 8Achcar RO, Yung GL, SalTer H ,et al. Morphologic changes in explanted lungs after prostacyclin therapy for pulmonary hypertension [ J ]. Eur J Med Res ,2006,11 ( 5 ) :203 - 207. 被引量:1
  • 9Opitz CF, Ewert R. Dual ET( A )/ET( B ) vs. selective ET( A ) endothelin receptor antagonism in patients with pulmonary hypertension [ J ]. Eur J Clin Invest ,2006,36( suppl 3 ) : 1 - 9. 被引量:1
  • 10Jacobs A, Preston IR, Gomberg - Maitland M. Endothelin receptor antagonism in pulmonary arterial hypertension - a role for selective ET ( A ) inhibition [ J ] ? Curt Med Res Opin ,2006,22 ( 12 ) :2567 - 2574. 被引量:1

共引文献5

同被引文献25

  • 1倪布清,张石江,朱煜明,张宁,王虹,解卫平.新型KATP通道开放剂埃他卡林对人肺动脉平滑肌细胞增殖的影响[J].国际呼吸杂志,2007,27(12):903-906. 被引量:5
  • 2Dias-Junior CA, Can SB, Tanus-Santos JE. Role of nitric oxide in the control of the pulmonary circulation:physiologi- cal, pathophysiological, and therapeutic implications [ J ]. J Bras Pneumol, 2008, 34(6) :412-419. 被引量:1
  • 3Diao YG, Jin Q, zhou J, et al.Transplantation of endothehal progenitor cells transfected with the eNOS gene for the therapy of hypoxic pulmonary hypertension in the rat[J]. Br J Anaesth, 2012, 108(3) :548. 被引量:1
  • 4Zong F, Zuo XR, Wang Q, et al. Iptakalim rescues human pulmonary artery endothelial cells from hypoxia induced nitric oxide system dysfunction [ J ]. Exp Ther Med, 2012, 5(3) :535-539. 被引量:1
  • 5Junbao D, Hui Y, Bing W, et al. Effect of L-arginine on collagen of high flow-induced pulmomary arterial remodeling [ J ]. Cite J, 2005, 69 (5) :603-608. 被引量:1
  • 6Perros F, Dorfmiiller P, Humbert M. Current insights on the pathogenesis of pulmonary arterial hypertension [ J ]. Semin Respir Crit Care Med, 2005, 26(4) :355-364. 被引量:1
  • 7Luke T, Maylor J, Undem C, et al. Kinase-dependent acti- vation of voltage-gated Ca2+channels by ET-1 in pulmonary anerial myocytes during chronic hypoxia [ J ]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(10) :L1128-L1 139. 被引量:1
  • 8Olave N, Nicola T, Zhang W, et al. Transforming growth factor-beta regulates endothehn-1 signaling in the newbom mouse lung during hypoxia exposure [ J ]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(9) :L857-L865. 被引量:1
  • 9Chuang IC, Dong HP, Yang RC, et al. Effect of carbon di- oxide on pulmonary vascular tone at various pulmonary arterial pressure levels induced by endothelin-1 [ J]. Lung, 2010, 188(3) :199-207. 被引量:1
  • 10梅宏波,左祥荣,解卫平,王虹.K_(ATP)通道与人肺动脉平滑肌细胞外信号调节激酶磷酸化的关系[J].实用老年医学,2009,23(2):100-103. 被引量:2

二级引证文献3

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