Skip Navigation


Cardiovascular Research Advance Access originally published online on December 4, 2007
Cardiovascular Research 2008 78(2):223-231; doi:10.1093/cvr/cvm086
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
78/2/223    most recent
cvm086v3
cvm086v2
cvm086v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Murakami, M.
Right arrow Articles by Simons, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murakami, M.
Right arrow Articles by Simons, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Non-canonical fibroblast growth factor signalling in angiogenesis

Masahiro Murakami*, Arye Elfenbein and Michael Simons

Angiogenesis Research Center and Section of Cardiology, Department of Medicine, and Department of Pharmacology and Toxicology, Dartmouth Medical School, Lebanon, NH 03756, USA

* Corresponding author. Tel: +1 603 650 2631; fax: +1 603 653 0510. E-mail address: masahiro.murakami{at}dartmouth.edu

Whereas fibroblast growth factors (FGFs) classically transmit their signals via high-affinity tyrosine kinase receptors (FGFR1–4), recent evidence strongly implicates non-tyrosine kinase receptors (NTKR) or cell-surface FGFR-interacting proteins as important players in FGF signalling. Although NTKR have lower affinity for FGFs in comparison with cognate tyrosine kinase receptors, because of their high abundance they can effectively bind FGFs and produce unique biological effects independent of FGFRs. A prime example of such NTKR is the syndecan family of plasma membrane proteoglycans and, in particular, syndecan-4, which transmits FGF signalling via a protein kinase C{alpha} pathway. Another NTKR, {alpha}vβ3 integrin, functions as an FGF signalling modulator by binding both FGF2 and FGFR1. Yet another NTKR, neural cell adhesion molecule (NCAM), can serve as an FGFR ligand and assemble an FGFR signalling complex in the absence of FGFs. Furthermore, N-cadherin, which has been reported to associate with FGFR, appears to activate FGFR in both ligand (FGF)-dependent and ligand-independent manners. Finally, gangliosides are implicated as a co-receptor system of FGFs. The biological consequence of non-canonical FGF signalling tends to be less discernable compared to the canonical FGFR activation because of the overlap between these two pathways; nevertheless, non-canonical signalling is important and sometimes essential for cellular functions. Given the diversity of FGF activities through embryonic development to adult physiology, the existence of the non-canonical signalling system may account for the different cellular response to the FGF input in different biological contexts. In this review, we will discuss recent findings related to non-canonical FGF signalling with emphasis on the endothelial biology and angiogenesis.

KEYWORDS Angiogenesis; Cadherins; Growth factors; FGF; NCAM; Signal transduction; Syndecan-4

Time for primary review: 25 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
J.-S. Silvestre, B. I. Levy, and A. Tedgui
Mechanisms of angiogenesis and remodelling of the microvasculature
Cardiovasc Res, May 1, 2008; 78(2): 201 - 202.
[Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.