[1]张利民,包秀丽.Sprouty调控转化生长因子-β信号通路介导的上皮间充质转化抑制后囊膜混浊的研究进展[J].眼科新进展,2019,39(7):690-694.[doi:10.13389/j.cnki.rao.2019.0159]
 ZHANG Li-Min,BAO Xiu-Li.Research progress of Sprouty regulates transform growth factor-β signaling pathway mediated epithelial mesenchymal transition and inhibits posterior capsular opacification[J].Recent Advances in Ophthalmology,2019,39(7):690-694.[doi:10.13389/j.cnki.rao.2019.0159]
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Sprouty调控转化生长因子-β信号通路介导的上皮间充质转化抑制后囊膜混浊的研究进展/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
39卷
期数:
2019年7期
页码:
690-694
栏目:
文献综述
出版日期:
2019-07-05

文章信息/Info

Title:
Research progress of Sprouty regulates transform growth factor-β signaling pathway mediated epithelial mesenchymal transition and inhibits posterior capsular opacification
作者:
张利民包秀丽
010100 内蒙古自治区呼和浩特市,内蒙古医科大学附属医院(张利民);内蒙古医科大学附属医院眼科(包秀丽)
Author(s):
ZHANG Li-MinBAO Xiu-Li
Affiliated Hospital of Inner Mongolia Medical University(ZHANG Li-Min),Hohhot 010100,Inner Mongolia Autonomous Region,China;Department of Ophthalmology,the Affiliated Hospital of Inner Mongolia Medical University(BAO Xiu-Li),Hohhot 010100,Inner Mongolia Autonomous Region,China
关键词:
Sprouty后囊膜混浊上皮间充质转化转化生长因子-β晶状体上皮细胞MAPK信号转导通路白内障
Keywords:
Sproutyposterior capsular opacificationepithelial mesenchymal transitionTGF- βlens epithelial cellsMAPK signaling pathwayscataract
分类号:
R776.1
DOI:
10.13389/j.cnki.rao.2019.0159
文献标志码:
A
摘要:
后囊膜混浊 (posterior capsular opacification,PCO) 是白内障手术的主要远期并发症,是由于手术切除纤维块后残留在囊袋中的晶状体上皮细胞(lens epithelial cell,LEC)的异常生长引起的。在成人术后2~5 a的发生率为20%~40%,儿童几乎为100%。大量研究表明LEC的上皮间充质转化(epithelial mesenchymal transition,EMT)及增殖过程是PCO发展的主要病理改变,转化生长因子-β(transform growth factor-β,TGF-β)信号通路参与了LEC的EMT过程,其包括经典的Smad信号通路及非Smad信号通路。丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路为主要的非Smad信号通路。Sprouty是RTK介导的Ras/ERK/MAPK 信号通路特异的抑制蛋白,并作为TGF-β诱导的EMT的负性调节因子抑制ERK信号通路,从而抑制EMT过程。本文将总结在PCO中LEC的EMT过程,以及Sprouty通过抑制TGF相关信号通路阻断PCO过程进行综述。
Abstract:
Posterior capsular opacification (PCO) is a major long-term complication of cataract surgery,and is caused by aberrant growth of lens epithelial cells(LECs) that are left behind in the capsular bag after surgical removal of the fiber mass.The incidence of postoperative 2-5 years is approximately 20%-40% in adults and almost 100% in children.A large number of studies have shown that epithelial mesenchymal transition (EMT) and proliferation of LECs are the main pathological changes in the development of PCO.TGF-β signaling pathway is involved in the EMT process of LECs.TGF- β signaling pathway includes canonical Smad signaling pathway and non Smad signaling pathway.The mitogen-activated protein kinase (MAPK) signaling pathway is the main non Smad signaling pathway.Sprouty is a specific inhibitor of the RTK-mediated Ras/ERK/MAPK signaling pathway and acts as a negative regulator of TGF-β induced EMT by inhibiting the ERK signaling pathway to inhibit the EMT process.A better understanding of the key cellular processes and molecular mechanisms of PCO may help to reduce the incidence of PCO,and the study of Sprouty may provide a useful therapeutic target for the prevention of EMT and cataract in the future.This review summarizes the EMT process of lens epithelial cells in PCO and Sprouty blocks the PCO process by inhibiting TGF-related signaling pathways.

参考文献/References:

[1] ZHANG B,CHEN Y,QIU M,DING Z.Long noncoding RNA expression profile in HLEB-3 cells during TGF-β2-induced epithelial-mesenchymal transition[J].BMC Ophthalmol,2017,17(1):69.
[2] ZHANG R,WEI Y H,ZHAO C Y,SONG H Y,SHEN N,CUI X.EDIL3 depletion suppress epithelial-mesenchymal transition of lens epithelial cells via transforming growth factor β pathway[J].Int J Ophthalmol,2018,11(1):18-24.
[3] LIU L,XIAO W.Notch1 signaling induces epithelial-mesenchymal transition in lens epithelium cells during hypoxia[J].BMC Ophthalmol,2017,17(1):135.
[4] CHEN X,XIAO W,CHEN W,LUO L,YE S,LIU Y.The epigenetic modifier trichostatin A,a histone deacetylase inhibitor,suppresses proliferation and epithelial-mesenchymal transition of lens epithelial cells[J].Cell Death Dis,2013,4:e884.
[5] ILIESCU I M,CONSTANTIN M A,COZMA C,MORARU O M,MORARU C M.Posterior capsule opacification and Nd-YAG rates evaluation in a large series of pseudophakic cases[J].Rom J Ophthalmol,2017,61(4):267-274.
[6] IZDEBSKA M,ZIELI N ′ SKA W,GRZANKA D,GAGAT M.The role of actin dynamics and actin-binding proteins expression in epithelial-to-mesenchymal transition and its association with cancer progression and evaluation of possible therapeutic targets[J].Biomed Res Int,2018,2018:4578373.
[7] SAVAGNER P.The epithelial-mesenchymal transition (EMT) phenomenon[J].Ann Oncol,2010,21 (Supplement 7):vii89-92.
[8] WANG Z,LI Y,KONG D,SARKAR F H.The role of notch signaling pathway in epithelial-mesenchymal transition (EMT) during development and tumor aggressiveness[J].Curr Drug Targets,2010,11(6):745-751.
[9] DONG N,TANG X,XU B.miRNA-181a inhibits the proliferation,migration,and epithelial-mesenchymal transition of lens epithelial cells [J].Invest Ophthalmol Vis Sci,2015,56(2):993-1001.
[10] CHO H J,YOO J.Rho activation is required for transforming growth factor-β-induced epithelial-mesenchymal transition in lens epithelial cells.[J].Cell Biol Int,2007,31(10):1225-1230.
[11] BAO X L,SONG H,CHEN Z,TANG X.Wnt3a promotes epithelial-mesenchymal transition,migration,and proliferation of lens epithelial cells[J].Mol Vis,2012,18:1983-1990.
[12] LIU T,ZHANG L,WANG Y,ZHANG H,LI L,BAO X.Dickkopf-1 inhibits Wnt3a-induced migration and epithelial-mesenchymal transition of human lens epithelial cells[J].Exp Eye Res,2017,161:43-51.
[13] ZHANG Y E.Non-smad signaling pathways of the TGF-β family[J].Cold Spring Harb Perspect Biol,2017,9(2):pii:a022129.
[14] DE IONGH R U,WEDERELL E,LOVICU F J,MCAVOY J W.Transforming growth factor-β-induced epithelial-mesenchymal transition in the lens:a Model for cataract formation[J].Cells Tissues Organs,2005,179(1-2):43-55.
[15] SAIKA S,YAMANAKA O,OKADA Y,TANAKA S,MIYAMOTO T,SUMIOKA T,et al.TGF-β in fibroproliferative diseases in the eye[J].Front Biosci (Schol Ed),2009,1:376-390.
[16] HAYASHIDA T,DECAESTECKER M,SCHNAPER H W.Cross-talk between ERK MAP kinase and Smad-signaling pathways enhances TGF-β dependent responses in human mesangial cells[J].FASEB J,2003,17(11):1576-1578.
[17] WATANABE-TAKANO H,TAKANO K,HATANO M,TOKUHISA T,ENDO T.DA-Raf-Mediated suppression of the Ras-ERK pathway is essential for TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial Type 2 cells[J].PLoS One,2015,10(5):e0127888.
[18] TAN X,ZHU Y,CHEN C,CHEN X,QIN Y,QU B,et al.Sprouty2 suppresses epithelial-mesenchymal transition of human lens epithelial cells through blockade of Smad2 and ERK1/2 pathways[J].PLoS One,2016,11(7):e0159275.
[19] RAO S,ZAIDI S,BANERJEE J,JOGUNOORI W,SEBASTIAN R,MISHRA B,et al.Transforming growth factor-β in liver cancer stem cells and regeneration[J].Hepatol Commun,2017,1(6):477-493.
[20] SHIN E H,BASSON M A,ROBINSON M L,MCAVOY J W,LOVICU F J.Sprouty is a negative regulator of transforming growth factor β-induced epithelial-to-mesenchymal transition and cataract[J].Mol Med,2012,18:861-873.
[21] XU J,LAMOUILLE S,DERYNCK R.TGF-β-induced epithelial to mesenchymal transition[J].Cell Res,2009,19:156-172.
[22] LEE M K,PARDOUX C,HALL M C,LEE P S,WARBURTON D,QING J,et al.TGF-β activates Erk MAP kinase signalling through direct phosphorylation of ShcA[J].EMBO J,2007,26(17):3957-3967.
[23] GUO X,WANG X F.Signaling cross-talk between TGF-β/BMP and other pathways ng[J].Cell Res,2009,19(1):71-88.
[24] LIU B,SUN J,LEI X,ZHU Z,PEI C,QIN L.MicroRNA-486-5p suppresses TGF-β2-induced proliferation,invasion and epithelial-mesenchymal transition of lens epithelial cells by targeting Smad2[J].J Biosci,2017,42(4):575-584.
[25] PEI C,MA B,KANG Q Y,QIN L,CUI L J.Effects of transforming growth factor β2 and connective tissue growth factor on induction of epithelial mesenchymal transition and extracellular matrix synthesis in human lens epithelial cells[J].Int J Ophthalmol,2013,6(6):752-757.
[26] CHEN X,YE S,XIAO W,WANG W,LUO L,LIU Y.ERK1/2 pathway mediates epithelial-mesenchymal transition by cross-interacting with TGFβ/Smad and Jagged/Notch signaling pathways in lens epithelial cells[J].Int J Mol Med,2014,33(6):1664-1670.
[27] CABRITA M A,CHRISTOFORI G.Sprouty proteins,masterminds of receptor tyrosine kinase signaling[J].Angiogenesis,2008,11(1):53-62.
[28] MEREDITH A.TENNIS,MICHELLE M.VAN SCOYK,SCOTT V.FREEMAN,KATHERINE M.VANDERVEST,RAPHAEL A.NEMENOFF,ROBERT A.WINN.Sprouty-4 inhibits transformed cell growth,migration and invasion,and epithelial-mesenchymal transition,and is regulated by Wnt7A through PPAR(Y) in non-small cell lung cancer[J].Mol Cancer Res,2010,8(6):833-843.
[29] KURACHA M R,SIEFKER E,LICHT J D,GOVINDARAJAN V.Spry1 and Spry2 are necessary for eyelid closure[J].Dev Biol,2013,383(2):227-238.
[30] BOROS J,NEWITT P,WANG Q,MCAVOY J W,LOVICU F J.Sef and Sprouty expression in the developing ocular lens:implications for regulating lens cell proliferation and differentiation [J].Semin Cell Dev Biol,2006,17(6):741-752.
[31] ZHAO G,BAILEY C G,FENG Y,RASKO J,LOVICU F J.Negative regulation of lens fiber cell differentiation by RTK antagonists Spry and Spred[J].Exp Eye Res,2018,170:148-159.
[32] MASON J M,MORRISON D J,BASSON M A,LICHT J D.Sprouty proteins:multifaceted negative-feedback regulators of receptor tyrosine kinase signaling[J].Trends Cell Biol,2006,16(1):45-54.
[33] MASOUMI-MOGHADDAM S,AMINI A,MORRIS D L.The developing story of Sprouty and cancer[J].Cancer Metastasis Rev,2014,33(2-3):695-720.
[34] ZHAO G,WOJCIECHOWSKI M C,JEE S,BOROS J,MCAVOY J W,LOVICU F J.Negative regulation of TGFβ-induced lens epithelial to mesenchymal transition (EMT) by RTK antagonists[J].Exp Eye Res,2015,132:9-16.

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备注/Memo

备注/Memo:
国家自然科学基金资助(编号:81360145)
更新日期/Last Update: 2019-07-01