What mouse mutants teach us about extracellular matrix function

被引:127
作者
Aszodi, A. [1 ]
Legate, Kyle R.
Nakchbandi, I.
Faessler, R.
机构
[1] Max Planck Inst Biochem, Dept Mol Med, D-85152 Martinsried, Germany
[2] Heidelberg Univ, Inst Immunol, D-69120 Heidelberg, Germany
关键词
gene targeting; transgenics; connective tissue; basement membrane; mouse development;
D O I
10.1146/annurev.cellbio.22.010305.104258
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
For many years the extracellular matrix was viewed as a benign scaffold for arranging cells within connective tissues, but it is now being redefined as a dynamic, mobile, and flexible key player in defining cellular behavior. Gene targeting, transgene expression, and spontaneous mutations of extracellular matrix proteins in mice have greatly accelerated our mechanistic view of the structural and instructive functions of the extracellular matrix in developmental and regenerative processes. This review summarizes the phenotypes of genetic mouse models carrying mutations in extracellular matrix proteins, with specific emphasis on recent advances. The application of reverse genetics has demonstrated the multi functionality of matrix proteins in a biological context and, in addition, has brought a novel perspective to the understanding of human pathologies.
引用
收藏
页码:591 / 621
页数:31
相关论文
共 157 条
[1]   Proteolysis of cell-surface tissue transglutaminase by matrix metalloproteinase-2 contributes to the adhesive defect and matrix abnormalities in thrombospondin-2-null fibroblasts and mice [J].
Agah, A ;
Kyriakides, TR ;
Bornstein, P .
AMERICAN JOURNAL OF PATHOLOGY, 2005, 167 (01) :81-88
[2]   The lack of thrombospondin-1 (TSP1) dictates the course of wound healing in double-TSP1/TSP2-null mice [J].
Agah, A ;
Kyriakides, TR ;
Lawler, J ;
Bornstein, P .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 161 (03) :831-839
[3]   Angiostatic peptides use plasma fibronectin to home to angiogenic vasculature [J].
Åkerman, ME ;
Pilch, J ;
Peters, D ;
Ruoslahti, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (06) :2040-2045
[4]   Matricellular proteins: Extracellular modulators of bone development, remodeling, and regeneration [J].
Alford, Andrea I. ;
Hankenson, Kurt D. .
BONE, 2006, 38 (06) :749-757
[5]   Mice deficient in small leucine-rich proteoglycans:: novel in vivo models for osteoporosis, osteoarthritis, Ehlers-Danlos syndrome, muscular dystrophy, and corneal diseases [J].
Ameye, L ;
Young, MF .
GLYCOBIOLOGY, 2002, 12 (09) :107R-116R
[6]   TARGETED MUTATION IN THE COL5A2 GENE REVEALS A REGULATORY ROLE FOR TYPE-V COLLAGEN DURING MATRIX ASSEMBLY [J].
ANDRIKOPOULOS, K ;
LIU, X ;
KEENE, DR ;
JAENISCH, R ;
RAMIREZ, F .
NATURE GENETICS, 1995, 9 (01) :31-36
[7]   Making sense of latent TGFβ activation [J].
Annes, JP ;
Munger, JS ;
Rifkin, DB .
JOURNAL OF CELL SCIENCE, 2003, 116 (02) :217-224
[8]   Structural and functional mutations of the perlecan gene cause Schwartz-Jampel syndrome, with myotonic myopathy and chondrodysplasia [J].
Arikawa-Hirasawa, E ;
Le, AH ;
Nishino, I ;
Nonaka, I ;
Ho, NC ;
Francomano, CA ;
Govindraj, P ;
Hassell, JR ;
Devaney, JM ;
Spranger, J ;
Stevenson, RE ;
Iannaccone, S ;
Dalakas, MC ;
Yamada, Y .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 70 (05) :1368-1375
[9]   Perlecan is essential for cartilage and cephalic development [J].
Arikawa-Hirasawa, E ;
Watanabe, H ;
Takami, H ;
Hassell, JR ;
Yamada, Y .
NATURE GENETICS, 1999, 23 (03) :354-358
[10]   Dyssegmental dysplasia, Silverman-Handmaker type, is caused by functional null mutations of the perlecan gene [J].
Arikawa-Hirasawa, E ;
Wilcox, WR ;
Le, AH ;
Silverman, N ;
Govindraj, P ;
Hassell, JR ;
Yamada, Y .
NATURE GENETICS, 2001, 27 (04) :431-434