Neuropilin-1 participates in wound angiogenesis

被引:51
作者
Matthies, AM
Low, QEH
Lingen, MW
DiPietro, LA
机构
[1] Loyola Univ, Med Ctr, Burn & Shock Trauma Inst, Maywood, IL 60153 USA
[2] Loyola Univ, Ctr Med, Dept Microbiol & Immunol, Maywood, IL 60153 USA
[3] Loyola Univ, Ctr Med, Dept Pathol, Maywood, IL 60153 USA
[4] Loyola Univ, Ctr Med, Dept Surg, Maywood, IL 60153 USA
关键词
D O I
10.1016/S0002-9440(10)64372-6
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Angiogenesis, the formation of new capillaries from existing vasculature, plays an essential role in tissue repair. The rapid onset and predominance of proangiogenic factors optimizes healing in damaged tissues. One factor that directly mediates wound vessel angiogenesis Is vascular endothelial growth factor (VEGF). Although much is known about the biology of VEGF and Its cognate receptors, VEGFR1 and VEGFR2, the role of a recently identified co-receptor for VEGF, neuropilin-1, is not well understood. Using a murine model of dermal wound repair, we found that neuropilin-1 was abundantly expressed on new vasculature in healing wounds. Moreover, mice treated with antineuropilin-1 antibodies exhibited a significant decrease in vascular density within these wounds (67% decrease, P = 0.0132). In in vitro assays, VEGF induced formation of endothelial cord-like structures on collagen get and endothelial cell migration toward VEGF was inhibited by antibodies directed against neuropilin-1. These results provide both in vitro and in vivo evidence for a critical role of neuropilin-1 in wound angiogenesis.
引用
收藏
页码:289 / 296
页数:8
相关论文
共 49 条
[1]   Isolation of putative progenitor endothelial cells for angiogenesis [J].
Asahara, T ;
Murohara, T ;
Sullivan, A ;
Silver, M ;
vanderZee, R ;
Li, T ;
Witzenbichler, B ;
Schatteman, G ;
Isner, JM .
SCIENCE, 1997, 275 (5302) :964-967
[2]  
BREIER G, 1992, DEVELOPMENT, V114, P521
[3]  
Brekken RA, 2000, CANCER RES, V60, P5117
[4]   EXPRESSION OF VASCULAR-PERMEABILITY FACTOR (VASCULAR ENDOTHELIAL GROWTH-FACTOR) BY EPIDERMAL-KERATINOCYTES DURING WOUND-HEALING [J].
BROWN, LF ;
YEO, KT ;
BERSE, B ;
YEO, TK ;
SENGER, DR ;
DVORAK, HF ;
VANDEWATER, L .
JOURNAL OF EXPERIMENTAL MEDICINE, 1992, 176 (05) :1375-1379
[5]  
BROWN LF, 1993, CANCER RES, V53, P4727
[6]   Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele [J].
Carmeliet, P ;
Ferreira, V ;
Breier, G ;
Pollefeyt, S ;
Kieckens, L ;
Gertsenstein, M ;
Fahrig, M ;
Vandenhoeck, A ;
Harpal, K ;
Eberhardt, C ;
Declercq, C ;
Pawling, J ;
Moons, L ;
Collen, D ;
Risau, W ;
Nagy, A .
NATURE, 1996, 380 (6573) :435-439
[7]  
Drevs J, 2000, CANCER RES, V60, P4819
[8]   Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene [J].
Ferrara, N ;
CarverMoore, K ;
Chen, H ;
Dowd, M ;
Lu, L ;
OShea, KS ;
PowellBraxton, L ;
Hillan, KJ ;
Moore, MW .
NATURE, 1996, 380 (6573) :439-442
[9]   Role of vascular endothelial growth factor in regulation of physiological angiogenesis [J].
Ferrara, N .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2001, 280 (06) :C1358-C1366
[10]   ANGIOGENESIS IN CANCER, VASCULAR, RHEUMATOID AND OTHER DISEASE [J].
FOLKMAN, J .
NATURE MEDICINE, 1995, 1 (01) :27-31