Paper - WANFANG MED ONLINE

You Position: Home > Paper

ADAMTS-7, a novel proteolytic culprit in vascular remodeling

( views:35, downloads:0 )

Author:: No author available

Journal Title:: ACTA PHYSIOLOGICA SINICA

Issue:: 4

DOI:: No doi available

Key Word:: ADAMTS-7;软骨寡聚基质蛋白;血管平滑肌;迁移;增殖;ADAMTS-7;COMP;vascular smooth muscle;migration;proliferation

Abstract： Vascular remodeling is being recognized as a fundamental process during atherosclerosis and restenosis. Cumulative studies have demonstrated that extracellular matrix (ECM) degrading enzymes play a critical role during vascular remodeling. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family is a recently identified metalloproteinase family which also has capacity to degrade ECM. ADAMTS family consists of 19 members and has been linked to a variety of physiological processes including development, angiogenesis, coagulation etc. Aberrant expression or function of ADAMTS members have been implicated to many disease states such as arthritis, cancer, thrombocytopenic purpura, but barely described with regard to cardiovascular disease. This review summarizes the recent advance with respect to the role of ADAMTS-7 in vascular remodeling. We review the structure, tissue distribution, substrate, expression and regulation of ADAMTS-7, especially highlight the fine tune by ADAMTS-7 of its substrate cartilage oligomeric matrix protein (COMP) in maintaining vascular homeostasis. By use of rat carotid artery balloon injury model to mimic vascular injury in vivo, we found that ADAMTS-7 protein was accumulated preferentially in neointima and mainly localized in vascular smooth muscle cells (VSMCs). Adenovirus-elicited ADAMTS-7 overexpression greatly accelerated VSMCs migration and proliferation both in vivo and in vitro, and subsequently aggravated neointima thickening post-injury. Conversely, siRNA-mediated ADAMTS-7 knock down bonafide inhibited VSMCs migration and proliferation in cultured VSMCs and injured arteries, and ultimately ameliorated neointima area. Further studies demonstrated that ADAMTS-7 facilitated VSMCs migration through degradation of its substrate COMP. Moreover, we elucidated that COMP has the capacity to maintain the contractile phenotype of VSMCs through interacting with integrin α7β1. ADAMTS-7 may therefore serve as a novel therapeutic target for atherosclerosis and postangioplasty restenosis.

Reference

[1]叶红燕,尹苗,商允菊,等.脂代谢相关基因在apoE基因缺失幼龄小鼠肝脏中的表达[J].2008,(1).
[2]Alain Colige,Aleksander L. Sieron,Shi-Wu Li,etc.Human Ehlers-Danlos Syndrome Type VII C and Bovine Dermatosparaxis Are Caused by Mutations in the Procollagen I N-Proteinase Gene[J].1999,65(2).
[3]Ross OH,Abbaszade I,Arner E,etc.Sites of aggrecan cleavage by recombinant human aggrecanase-1 (ADAMTS-4).[J].2000,275(24).
[4]Joost P G, Sluijter,Dominique P V, de Kleijn,Gerard, Pasterkamp.Vascular remodeling and protease inhibition--bench to bedside.[J].2006,69(3).
[5]Wang LW,Longpre JM,Somerville RP,etc.ADAMTS7B, the full-length product of the ADAMTS7 gene, is a chondroitin sulfate proteoglycan containing a mucin domain.[J].2004,279(34).
[6]Lijnen HR.Plasmin and matrix metalloproteinases in vascular remodeling.[J].2001,86(1).
[7]S, Uemura,H, Matsushita,W, Li,etc.Diabetes mellitus enhances vascular matrix metalloproteinase activity: role of oxidative stress.[J].2001,88(12).
[8]Murthy S,Ryan A,He C,etc.Rac1-mediated mitochondrial H2O2 generation regulates MMP-9 gene expression in macrophages via inhibition of SP-1 and AP-1.[J].2010,285(32).
[9]Apte SS.A disintegrin-like and metalloprotease (reprolysin-type) with thrombospondin type 1 motif (ADAMTS) superfamily: functions and mechanisms.[J].2009,284(46).
[10]Z S, Galis,M, Muszynski,G K, Sukhova,etc.Cytokine-stimulated human vascular smooth muscle cells synthesize a complement of enzymes required for extracellular matrix digestion.[J].1994,75(1).
[11]Lawler J,Fenchel M,Chen H,etc.Cartilage oligomeric matrix protein (thrombospondin-5) is expressed by human vascular smooth muscle cells.[J].2001,21(1).
[12]Liu CJ.The role of ADAMTS-7 and ADAMTS-12 in the pathogenesis of arthritis.[J].2009,5(1).
[13]Fernandes RJ,Colige A,Cohn DH,etc.Procollagen II amino propeptide processing by ADAMTS-3. Insights on dermatosparaxis.[J].2001,276(34).
[14]Somerville RP,Longpre JM,Jungers KA,etc.Characterization of ADAMTS-9 and ADAMTS-20 as a distinct ADAMTS subfamily related to Caenorhabditis elegans GON-1.[J].2003,278(11).
[15]Gottschall PaulE,Gao Gui,Westling Jennifer,etc.Activation of the proteolytic activity of ADAMTS4 (aggrecanase-1) by C-terminal truncation.[J].2002,277(13).
[16]A, Lafont,E, Durand,J L, Samuel,etc.Endothelial dysfunction and collagen accumulation: two independent factors for restenosis and constrictive remodeling after experimental angioplasty.[J].1999,100(10).
[17]Hu J,Van-den-Steen PE,Sang QX,etc.Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases.[J].2007,6(6).
[18]Hiroyuki, Hao,Giulio, Gabbiani,Marie-Luce, Bochaton-Piallat.Arterial smooth muscle cell heterogeneity: implications for atherosclerosis and restenosis development.[J].2003,23(9).
[19]Colome N,Rodriguez Manzaneque JC,Arribas J,etc.The cleavage of semaphorin 3C induced by ADAMTS1 promotes cell migration.[J].2010,285(4).
[20]L, Sottrup-Jensen.Alpha-macroglobulins: structure, shape, and mechanism of proteinase complex formation.[J].1989,264(20).
[21]Ortega MA,Lombardo M,Vazquez F,etc.METH-1, a human ortholog of ADAMTS-1, and METH-2 are members of a new family of proteins with angio-inhibitory activity.[J].1999,274(33).
[22]A, Tuuttila,E, Morgunova,U, Bergmann,etc.Three-dimensional structure of human tissue inhibitor of metalloproteinases-2 at 2.1 A resolution.[J].1998,284(4).
[23]Gendron C.,Itoh Y. Nagase H.,Kashiwagi M.,etc.Altered proteolytic activities of ADAMTS-4 expressed by C-terminal processing[J].2004,279(11).
[24]Shepherd J,Simonsen KL,Sacks FM,etc.Association between ADAMTS1 matrix metalloproteinase gene variation, coronary heart disease, and benefit of statin therapy.[J].2008,28(3).
[25]Esteller M,Cal S,Obaya AJ,etc.The ADAMTS12 metalloprotease gene is epigenetically silenced in tumor cells and transcriptionally activated in the stroma during progression of colon cancer.[J].2009,122(16).
[26]Gary SC,Matthews RT,Arner EC,etc.Brain-enriched hyaluronan binding (BEHAB)/brevican cleavage in a glioma cell line is mediated by a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family member.[J].2000,275(30).
[27]Zorina Galis,Chad Johnson,Denis Godin,etc.Targeted Disruption of the Matrix Metalloproteinase-9 Gene Impairs Smooth Muscle Cell Migration and Geometrical Arterial Remodeling[J].2002,91(9).
[28]Luan Y,Sehgal B,Yu S,etc.ADAMTS-12 associates with and degrades cartilage oligomeric matrix protein.[J].2006,281(23).
[29]Tan XY,Corcoran C,Jin M,etc.ADAMTS-8 exhibits aggrecanase activity and is expressed in human articular cartilage.[J].2004,23(4).
[30]Newby AC.Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture.[J].2005,85(1).
[31]Shi-Wu Li,Alain Colige,Aleksander L. Sieron.cDNA cloning and expression of bovine procollagen I N-proteinase: A new member of the superfamily of zinc-metalloproteinases with binding sites for cells and other matrix components[J].1997,94(6).
[32]Ross R.Atherosclerosis--an inflammatory disease.[J].1999,340(2).
[33]Lohi J,Wilson CL,Parks WC,etc.Epilysin, a novel human matrix metalloproteinase (MMP-28) expressed in testis and keratinocytes and in response to injury.[J].2001,276(13).
[34]Howell DR,Bai XH,Abramson SB,etc.Inhibition of ADAMTS-7 and ADAMTS-12 degradation of cartilage oligomeric matrix protein by alpha-2-macroglobulin.[J].2008,16(11).
[35]M D, Tortorella,T C, Burn,M A, Pratta,etc.Purification and cloning of aggrecanase-1: a member of the ADAMTS family of proteins.[J].1999,284(5420).
[36]Lebares CC,Lee S,Wang WM,etc.Transforming growth factor-beta induces secretion of activated ADAMTS-2. A procollagen III N-proteinase.[J].2003,278(21).
[37]H R, Lijnen,B, Van Hoef,I, Vanlinthout,etc.Accelerated neointima formation after vascular injury in mice with stromelysin-3 (MMP-11) gene inactivation.[J].1999,19(12).
[38]Owens GK.Regulation of differentiation of vascular smooth muscle cells.[J].1995,75(3).
[39]G G, Levy,W C, Nichols,E C, Lian,etc.Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura.[J].2001,413(6855).
[40]Sugimoto,K,Takahashi,M,Yamamoto,Y,etc.Identification of aggrecanase activity in medium of cartilage culture.[J].1999,126(2).
[41]A, Oldberg,P, Antonsson,K, Lindblom,etc.COMP (cartilage oligomeric matrix protein) is structurally related to the thrombospondins.[J].1992,267(31).
[42]Llamazares M,Obaya AJ,Heljasvaara R,etc.The ADAMTS12 metalloproteinase exhibits anti-tumorigenic properties through modulation of the Ras-dependent ERK signalling pathway.[J].2007,120(Pt.20).
[43]Tomás, Vaisar,Sean Y, Kassim,Ivan G, Gomez,etc.MMP-9 sheds the beta2 integrin subunit (CD18) from macrophages.[J].2009,8(5).
[44]Nishio K,Zheng X,Sadler JE,etc.Cleavage of von Willebrand factor requires the spacer domain of the metalloprotease ADAMTS13.[J].2003,278(32).
[45]D, Pei,S J, Weiss.Furin-dependent intracellular activation of the human stromelysin-3 zymogen.[J].1995,375(6528).
[46]Shuping Gao,Christian De Geyter,K.Kossowska,etc.FSH stimulates the expression of the ADAMTS-16 protease in mature human ovarian follicles[J].2007,13(7).
[47]Hisham S. Bassiouny,Ruo H. Song,Xue F. Hong,etc.Flow Regulation of 72-kD Collagenase IV (MMP-2) After Experimental Arterial Injury[J].1998,98(2).
[48]Murphy G,Edwards DR,Baker AH.Metalloproteinase inhibitors: biological actions and therapeutic opportunities.[J].2002,115(Pt.19).
[49]Deendayal Dinakarpandian,Keith Brew,Hideaki Nagase.Tissue inhibitors of metalloproteinases: evolution, structure and function[J].2000,1477(1).
[50]Plaza-Calonge-Mdel C,Iruela-Arispe ML,Rodriguez-Manzaneque JC,etc.Cleavage of syndecan-4 by ADAMTS1 provokes defects in adhesion.[J].2009,41(4).
[51]Li W,Li H,Challis JR,etc.Tumor necrosis factor stimulates matrix metalloproteinase 9 secretion from cultured human chorionic trophoblast cells through TNF receptor 1 signaling to IKBKB-NFKB and MAPK1/3 pathway.[J].2010,83(3).
[52]Beschin A,Van Beeumen J,Samyn B,etc.Characterization and partial amino acid sequencing of a 107-kDa procollagen I N-proteinase purified by affinity chromatography on immobilized type XIV collagen.[J].1995,270(28).
[53]Zhu Y,Bai X,Liu CJ,etc.ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries.[J].2009,104(5).