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中华妇幼临床医学杂志(电子版) ›› 2017, Vol. 13 ›› Issue (04) : 482 -485. doi: 10.3877/cma.j.issn.1673-5250.2017.04.020

所属专题: 文献

综述

细胞外基质在支气管肺发育不良发病机制中的作用
李淑君1, 吴升华1, 陈筱青1,()   
  1. 1. 210029 南京医科大学第一附属医院儿科
  • 收稿日期:2017-02-07 修回日期:2017-06-11 出版日期:2017-08-01
  • 通信作者: 陈筱青

Roles of extracellular matrix in bronchopulmonary dysplasia: research progress

Shujun Li1, Shenghua Wu1, Xiaoqing Chen1,()   

  1. 1. Department of Pediatrics, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
  • Received:2017-02-07 Revised:2017-06-11 Published:2017-08-01
  • Corresponding author: Xiaoqing Chen
  • About author:
    Corresponding author: Chen Xiaoqing, Email:
引用本文:

李淑君, 吴升华, 陈筱青. 细胞外基质在支气管肺发育不良发病机制中的作用[J]. 中华妇幼临床医学杂志(电子版), 2017, 13(04): 482-485.

Shujun Li, Shenghua Wu, Xiaoqing Chen. Roles of extracellular matrix in bronchopulmonary dysplasia: research progress[J]. Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition), 2017, 13(04): 482-485.

支气管肺发育不良(BPD)是发生于早产儿机械通气或氧疗后常见的慢性呼吸系统疾病。随着近年早产儿存活率的提高,BPD已成为新生儿重症监护病房的棘手问题之一。目前,BPD的发病机制尚未完全阐明,其可能与肺发育相关基因的协同表达、细胞通讯、物理作用力、细胞与细胞外基质(ECM)的相互作用受干扰有关。其中,ECM是存在于细胞间的动态网状结构,由纤维蛋白、糖蛋白复合物、ECM相关分子及ECM重构酶等构成,作为肺发挥正常功能的基础物质,十分重要。笔者拟就ECM在BPD发病机制中作用研究进展进行综述。

Bronchopulmonary dysplasia (BPD) is a kind of chronic lung diseases in premature infants after being treated with mechanical ventilation or oxygen therapy. With the development of neonatal survival rate, BPD has gradually become one of the most difficult problems in neonatal intensive care unit. Nowadays, the pathogenic mechanisms of BPD have not been well-elucidated. It may be associated with coordinated action of gene expression, cell-cell communication, physical forces, and cell interactions with the extracellular matrix (ECM), which involved in the regulation of normal lung development together. ECM is the dynamic mesh structure existing between cells, which consist of the structural protein, dystrophin-glycoprotein, fibrin, extracellular matrix molecules and remodeling enzymes. ECM plays an important role as the basis material of lung function. In this review, we will focus on the recent research progresses about the role of ECM in the pathogenesis of BPD.

[1]
Hawwa RL, Hokenson MA, Wang Y, et al. Differential expression of MMP-2 and -9 and their inhibitors in fetal lung cells exposed to mechanical stretch: regulation by IL-10 [J]. Lung, 2011, 189(4): 341-349.
[2]
Jobe AH. The new bronchopulmonary dysplasia [J]. Curr Opin Pediatr, 2011, 23(2): 167-172.
[3]
孙影,贾艳春,魏中秋,等. 细胞外信号调节激酶1/2通路在Peroxiredoxin-1抑制转化生长因子-β1诱导的Ⅰ、Ⅲ型胶原蛋白表达中的作用[J].中国现代医学杂志,2015, 25(26): 7-11.
[4]
Velten M, Britt RD Jr, Heyob KM, et al. Prenatal inflammation exacerbates hyperoxia-induced functional and structural changes in adult mice [J]. Am J Physiol Regul Integr Comp Physiol, 2012, 303(3): R279-R290.
[5]
张慧,富建华,薛辛东,等. 肌成纤维细胞在高氧致支气管肺发育不良新生大鼠肺组织中的分布特点及表达规律[J]. 沈阳师范大学学报(自然科学版), 2011, 29(2): 267-272.
[6]
张旭,谢敏,高艳,等. 低氧对大鼠肺组织结构的影响及其机制的探讨 [J].四川大学学报(医学版), 2012,43(1): 1-5.
[7]
刘秋彤,韩文莉,郭春宝,等. 弹性纤维系统在小鼠支气管肺发育不良中的动态表达规律 [J]. 第三军医大学学报,2014, 36(23): 2353-2357.
[8]
Mižíková I, Ruiz-Camp J, Steenbock H, et al. Collagen and elastin cross-linking is altered during aberrant late lung development associated with hyperoxia [J]. Am J Physiol Lung Cell Mol Physiol, 2015, 308(11): L1145-L1158.
[9]
Hilgendorff A, Parai K, Ertsey R, et al. Lung matrix and vascular remodeling in mechanically ventilated elastin haploinsufficient newborn mice [J]. Am J Physiol Lung Cell Mol Physiol, 2015, 308(5): L464-L478.
[10]
Kamei M, Miyajima A, Fujisawa M, et al. Effects of postnatal dexamethasone treatment on mRNA expression profiles of genes related to alveolar development in an emphysema model in mice [J]. J Toxicol Sci, 2014, 39(4): 665-670.
[11]
Han W, Guo C, Liu Q, et al. Aberrant elastin remodeling in the lungs of O2-exposed newborn mice; primarily results from perturbed interaction between integrins and elastin [J]. Cell Tissue Res, 2015, 359(2): 589-603.
[12]
Roth-Kleiner M, Berger TM, Gremlich S, et al. Neonatal steroids induce a down-regulation of tenascin-C and elastin and cause a deceleration of the first phase and an acceleration of the second phase of lung alveolarization [J]. Histochem Cell Biol, 2014, 141(1): 75-84.
[13]
Olave N, Lal CV, Halloran B, et al. Regulation of alveolar septation by microRNA-489 [J]. Am J Physiol Lung Cell Mol Physiol, 2016, 310(5): L476-L487.
[14]
Kaarteenaho-Wiik R, Kinnula VL, Herva R, et al. Tenascin-C is highly expressed in respiratory distress syndrome and bronchopulmonary dysplasia [J]. J Histochem Cytochem, 2002, 50(3): 423-431.
[15]
Zhang X, Xu J, Wang J, et al. Reduction of microRNA-206 contributes to the development of bronchopulmonary dysplasia through up-regulation of fibronectin 1 [J]. PLoS One, 2013, 8(9): e74750.
[16]
Watts CL, Fanaroff AA, Bruce MC. Elevation of fibronectin levels in lung secretions of infants with respiratory distress syndrome and development of bronchopulmonary dysplasia [J]. J Pediatr, 1992, 120(4 Pt 1): 614-620.
[17]
Sinkin RA, Roberts M, LoMonaco MB, et al. Fibronectin expression in bronchopulmonary dysplasia [J]. Pediatr Dev Pathol, 1998, 1(6): 494-502.
[18]
Kimura M, Hashimoto N, Kusunose M, et al. Exogenous induction of unphosphorylated PTEN reduces TGFβ-induced extracellular matrix expressions in lung fibroblasts [J]. Wound Repair Regen, 2017, 25(1): 86-97.
[19]
Han W, Guo C, Liu Q, et al. Aberrant elastin remodeling in the lungs of O2-exposed newborn mice; primarily results from perturbed interaction between integrins and elastin [J]. Cell Tissue Res, 2015, 359(2): 589-603.
[20]
Kroon AA, Wang J, Post M. Alterations in expression of elastogenic and angiogenic genes by different conditions of mechanical ventilation in newborn rat lung [J]. Am J Physiol Lung Cell Mol Physiol, 2015, 308(7): L639-L649.
[21]
Lin Z, Wang Z, Li G, et al. Fibulin-3 may improve vascular health through inhibition of MMP-2/9 and oxidative stress in spontaneously hypertensive rats [J]. Mol Med Rep, 2016, 13(5): 3805-3812.
[22]
Nguyen AD, Itoh S, Jeney V, et al. Fibulin-5 is a novel binding protein for extracellular superoxide dismutase [J]. Circ Res, 2004, 95(11): 1067-1074.
[23]
Sasaki T, Hanisch FG, Deutzmann R, et al. Functional consequence of fibulin-4 missense mutations associated with vascular and skeletal abnormalities and cutis laxa [J]. Matrix Biol, 2016, 56: 132-149.
[24]
Bland RD, Ertsey R, Mokres LM, et al. Mechanical ventilation uncouples synthesis and assembly of elastin and increases apoptosis in lungs of newborn mice. Prelude to defective alveolar septation during lung development? [J]. Am J Physiol Lung Cell Mol Physiol, 2008, 294(1): L3-L14.
[25]
Liu S, Parameswaran H, Young SM, et al. JNK suppresses pulmonary fibroblast elastogenesis during alveolar development [J]. Respir Res, 2014, 15(1): 34.
[26]
Han W, Guo C, Liu Q, et al. Aberrant elastin remodeling in the lungs of O2-exposed newborn mice; primarily results from perturbed interaction between integrins and elastin [J]. Cell Tissue Res, 2015, 359(2): 589-603.
[27]
Wang J, Bao L, Yu B, et al. Interleukin-1β promotes epithelial-derived alveolar elastogenesis via αvβ6 integrin-dependent TGF-β activation [J]. Cell Physiol Biochem, 2015, 36(6): 2198-2216.
[28]
Poonyagariyagorn HK, Metzger S, Dikeman D, et al. Superoxide dismutase 3 dysregulation in a murine model of neonatal lung injury [J]. Am J Respir Cell Mol Biol, 2014, 51(3): 380-390.
[29]
Lim R, Muljadi R, Koulaeva E, et al. Activin A contributes to the development of hyperoxia-induced lung injury in neonatal mice [J]. Pediatr Res, 2015, 77(6): 749-756.
[30]
Lee C, An J, Kim JH, et al. Low levels of tissue inhibitor of metalloproteinase-2 at birth may be associated with subsequent development of bronchopulmonary dysplasia in preterm infants [J]. Korean J Pediatr, 2015, 58(11): 415-420.
[31]
Xiao Q, Ge G. Lysyl oxidase, extracellular matrix remodeling and cancer metastasis[J]. Cancer Microenviron, 2012, 5(3): 261-273.
[32]
Greenlee KJ, Werb Z, Kheradmand F. Matrix metalloproteinases in lung: multiple, multifarious, and multifaceted [J]. Physiol Rev, 2007, 87(1): 69-98.
[33]
Niedermaier S, Hilgendorff A. Bronchopulmonary dysplasia: an overview about pathophysiologic concepts [J]. Mol Cell Pediatr, 2015, 2(1): 2.
[34]
Sasaki T, Stoop R, Sakai T, et al. Loss of fibulin-4 results in abnormal collagen fibril assembly in bone, caused by impaired lysyl oxidase processing and collagen cross-linking [J]. Matrix Biol, 2016, 50: 53-66.
[35]
Xia XD, Lee J, Khan S, et al. Suppression of phosphatidylinositol 3-kinase/Akt signaling attenuates hypoxia-induced pulmonary hypertension through the downregulation of lysyl oxidase [J]. DNA Cell Biol, 2016, 35(10): 599-606.
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