MT1-MMP regulates MMP-2 expression and angiogenesis-related functions in human umbilical vein endothelial cells

被引:19
作者
Lee, Hsinyu [1 ,2 ,5 ,6 ,7 ]
Chang, Kai-Wei [3 ]
Yang, Hsi-Yuan [3 ]
Lin, Po-Wei [2 ]
Chen, Shee-Uan [4 ]
Huang, Yuan-Li [8 ]
机构
[1] Natl Taiwan Univ, Dept Life Sci, Taipei 10764, Taiwan
[2] Natl Taiwan Univ, Inst Zool, Taipei 10764, Taiwan
[3] Natl Taiwan Univ, Inst Mol & Cellular Biol, Taipei 10764, Taiwan
[4] Natl Taiwan Univ Hosp, Dept Obstet & Gynecol, Taipei 100, Taiwan
[5] Natl Taiwan Univ, Ctr Biotechnol, Taipei 10764, Taiwan
[6] Natl Taiwan Univ, Angiogenesis Res Ctr, Taipei 10764, Taiwan
[7] Natl Taiwan Univ, Res Ctr Dev Biol & Regenerat Med, Taipei 10764, Taiwan
[8] Asia Univ, Coll Hlth Sci, Dept Biotechnol, Taichung, Taiwan
关键词
MT1-MMP; MMP-2; HUVECs; Angiogenesis; MEMBRANE-TYPE-1; MATRIX-METALLOPROTEINASE; 1-MATRIX METALLOPROTEINASE; MYOCARDIAL-INFARCTION; TUMOR ANGIOGENESIS; TARGETED DELETION; TISSUE INHIBITOR; ACTIVATION; GROWTH; MECHANISM; SURFACE;
D O I
10.1016/j.bbrc.2013.06.046
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Membrane type 1 (MT1)-MMP is a member of matrix metalloproteinases (MMPs) that regulates extracellular matrix remodeling. In addition, MT1-MMP also serves as a multi-functional protein. However, the functional role of MT1-MMP in human endothelial cells remains unclear. In this study we use real-time PCR and Western blotting to demonstrate for the first time that MMP-2 expression is regulated by MT1-MMP in human endothelial cells. Moreover, MMP-2 activity is also modulated by MT1-MMP. In addition we found that endothelial cells, ECM adhesion and human endothelial cell tube formation, which are known to be regulated by MMP-2, are blocked by MT1-MMP siRNA. These results suggest that MT1-MMP plays an important role in regulating angiogenesis in human endothelial cells. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:232 / 238
页数:7
相关论文
共 32 条
[1]  
Bottos A., 2013, CELL MOL LI IN PRESS
[2]   Mechanisms of angiogenesis and arteriogenesis [J].
Carmeliet, P .
NATURE MEDICINE, 2000, 6 (04) :389-395
[3]   Angiogenesis in cancer and other diseases [J].
Carmeliet, P ;
Jain, RK .
NATURE, 2000, 407 (6801) :249-257
[4]   Tissue inhibitor of metalloproteinases-2 binding to membrane-type 1 matrix metalloproteinase induces MAPK activation and cell growth by a non-proteolytic mechanism [J].
D'Alessio, Silvia ;
Ferrari, Giovanni ;
Cinnante, Karma ;
Scheerer, William ;
Galloway, Aubrey C. ;
Roses, Daniel F. ;
Rozanov, Dmitri V. ;
Remacle, Albert G. ;
Oh, Eok-Soo ;
Shiryaev, Sergey A. ;
Strongin, Alex Y. ;
Pintucci, Giuseppe ;
Mignatti, Paolo .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2008, 283 (01) :87-99
[5]   Matrix Metalloproteinase-2-deficient Fibroblasts Exhibit an Alteration in the Fibrotic Response to Connective Tissue Growth Factor/CCN2 because of an Increase in the Levels of Endogenous Fibronectin [J].
Droppelmann, Cristian A. ;
Gutierrez, Jaime ;
Vial, Cecilia ;
Brandan, Enrique .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (20) :13551-13561
[6]   Functional interplay between endothelial nitric oxide synthase and membrane type 1-matrix metalloproteinase in migrating endothelial cells [J].
Genis, Laura ;
Gonzalo, Pilar ;
Tutor, Antonio S. ;
Galvez, Beatriz G. ;
Martinez-Ruiz, Antonio ;
Zaragoza, Carlos ;
Lamas, Santiago ;
Tryggvason, Karl ;
Apte, Suneel S. ;
Arroyo, Alicia G. .
BLOOD, 2007, 110 (08) :2916-2923
[7]   Regulation of matrix metalloproteinase activity in health and disease [J].
Hadler-Olsen, Elin ;
Fadnes, Bodil ;
Sylte, Ingebrigt ;
Uhlin-Hansen, Lars ;
Winberg, Jan-Olof .
FEBS JOURNAL, 2011, 278 (01) :28-45
[8]   Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction [J].
Hayashidani, S ;
Tsutsui, H ;
Ikeuchi, M ;
Shiomi, T ;
Matsusaka, H ;
Kubota, T ;
Imanaka-Yoshida, K ;
Itoh, T ;
Takeshita, A .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 285 (03) :H1229-H1235
[9]   Membrane type I matrix metalloproteinase usurps tumor growth control imposed by the three-dimensional extracellular matrix [J].
Hotary, KB ;
Allen, ED ;
Brooks, PC ;
Datta, NS ;
Long, MW ;
Weiss, SJ .
CELL, 2003, 114 (01) :33-45
[10]  
Jo Y, 2000, BIOCHEM J, V345, P511, DOI 10.1042/bj3450511