Role of fibroblast growth factor signaling in vascular formation and maintenance: orchestrating signaling networks as an integrated system

被引:12
作者
Murakami, Masahiro [1 ]
Sakurai, Takashi [1 ]
机构
[1] Yale Univ, Sch Med, Yale Cardiovasc Res Ctr, Sect Cardiovasc Med,Dept Internal Med, New Haven, CT 06520 USA
关键词
BLOOD-BRAIN-BARRIER; FACTOR-INDUCED ANGIOGENESIS; CELL-CELL ADHESION; N-CADHERIN; ENDOTHELIAL-CELLS; FGF-RECEPTOR; TUMOR-GROWTH; THERAPEUTIC NEOVASCULARIZATION; DEPENDENT REGULATION; FACTOR EXPRESSION;
D O I
10.1002/wsbm.1190
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The vascular system has begun to be perceived as a dynamic organ actively controlling a wide variety of physiological processes. The structural and functional integrity of blood vessels, regulated by signaling activities finely modulating cellcell and cellmatrix interactions, is crucial for vessel physiology, as well as basic functionality of the tissue. Throughout the process of new vessel formation, while blood vessels are actively reorganized and remodeled with migration and proliferation of vascular cells, maintenance of vascular barrier function is essentially important. These conflicting properties, i.e., dynamic cellular mobilization and maintenance of barrier integrity, are simultaneously achieved through the interaction of highly organized signaling networks governing coordinated cellcell interplay. Recent evidence suggests that the fibroblast growth factor (FGF) system plays a regulatory role in several physiological conditions in the vascular system. In this article, we will attempt to summarize current knowledge in order to understand the mechanism of this coordination and evaluate the pivotal role of FGF signaling in integrating a diverse range of signaling events in vascular growth and maintenance. WIREs Syst Biol Med 2012, 4:615629. DOI: 10.1002/wsbm.1190 For further resources related to this article, please visit the WIREs website. Conflict of interest: The authors have declared that no conflict of interest exists.
引用
收藏
页码:615 / 629
页数:15
相关论文
共 124 条
[1]   VE-Cadherin-Mediated Cell-Cell Interaction Suppresses Sprouting via Signaling to MLC2 Phosphorylation [J].
Abraham, Sabu ;
Yeo, Margaret ;
Montero-Balaguer, Mercedes ;
Paterson, Hugh ;
Dejana, Elisabetta ;
Marshall, Christopher J. ;
Mavria, Georgia .
CURRENT BIOLOGY, 2009, 19 (08) :668-674
[2]   Brivanib, a Dual FGF/VEGF Inhibitor, Is Active Both First and Second Line against Mouse Pancreatic Neuroendocrine Tumors Developing Adaptive/Evasive Resistance to VEGF Inhibition [J].
Allen, Elizabeth ;
Walters, Ian B. ;
Hanahan, Douglas .
CLINICAL CANCER RESEARCH, 2011, 17 (16) :5299-5310
[3]   VASCULAR ENDOTHELIAL GROWTH-FACTOR ACTS AS A SURVIVAL FACTOR FOR NEWLY FORMED RETINAL-VESSELS AND HAS IMPLICATIONS FOR RETINOPATHY OF PREMATURITY [J].
ALON, T ;
HEMO, I ;
ITIN, A ;
PEER, J ;
STONE, J ;
KESHET, E .
NATURE MEDICINE, 1995, 1 (10) :1024-1028
[4]   Growth factor-induced therapeutic angiogenesis in the heart: protein therapy [J].
Annex, BH ;
Simons, M .
CARDIOVASCULAR RESEARCH, 2005, 65 (03) :649-655
[5]   Expression pattern of fibroblast growth factors (FGFs), their receptors and antagonists in primary endothelial cells and vascular smooth muscle cells [J].
Antoine, M ;
Wirz, W ;
Tag, CG ;
Mavituna, M ;
Emans, N ;
Korff, T ;
Stoldt, V ;
Gressner, AM ;
Kiefer, P .
GROWTH FACTORS, 2005, 23 (02) :87-95
[6]   Targeted disruption of fibroblast growth factor (FGF) receptor 2 suggests a role for FGF signaling in pregastrulation mammalian development [J].
Arman, E ;
Haffner-Krausz, R ;
Chen, Y ;
Heath, JK ;
Lonai, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (09) :5082-5087
[7]   Endothelial/pericyte interactions [J].
Armulik, A ;
Abramsson, A ;
Betsholtz, C .
CIRCULATION RESEARCH, 2005, 97 (06) :512-523
[8]   Pericytes regulate the blood-brain barrier [J].
Armulik, Annika ;
Genove, Guillem ;
Mae, Maarja ;
Nisancioglu, Maya H. ;
Wallgard, Elisabet ;
Niaudet, Colin ;
He, Liqun ;
Norlin, Jenny ;
Lindblom, Per ;
Strittmatter, Karin ;
Johansson, Bengt R. ;
Betsholtz, Christer .
NATURE, 2010, 468 (7323) :557-U231
[9]  
Auguste P, 2001, CANCER RES, V61, P1717
[10]   Cellular changes in normal blood capillaries undergoing regression after inhibition of VEGF signaling [J].
Baffert, F ;
Le, T ;
Sennino, B ;
Thurston, G ;
Kuo, CJ ;
Hu-Lowe, D ;
McDonald, DM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 290 (02) :H547-H559