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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:883.)
© 2005 American Heart Association, Inc.

Editorials

FGFR1 and the Bloodline of the Vasculature

Victor W.M. van Hinsbergh; Ton J. Rabelink

From the Laboratory for Physiology (V.W.M.w.H.), Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, and the Department of Nephrology (T.J.R.), Leiden University Medical Center, Leiden, The Netherlands.

Correspondence to Victor W.M. van Hinsbergh, PhD, Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. E-mail v.vanhinsbergh@vumc.nl

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Since the recognition of basicfibroblast growth factor (bFGF, FGF-2) and acidic FGF (aFGF, FGF-1) as proliferation and maintenance factors for endothelial cells in culture,^1,2 much interest has arisen regarding their role as potential angiogenic factors in tumors and tissue healing in vivo. The FGFs, of which presently at least 22 members have been recognized,³ interact with FGF receptors (FGFRs). After FGF binding, the FGFRs dimerize and become activated displaying protein tyrosine kinase activity and subsequent signaling in the cell.^4,5 Four functional FGFRs have been recognized, FGFR1–4, most of which can be encountered in various alternative spliced isoforms. FGFR1 plays an essential role during early stages of development of the mesoderm and at several levels during organogenesis.^3,6 FGF/FGFR1 is expressed almost exclusively in the mesenchyme, including endothelial cells, smooth muscle cells, and hemopoietic progenitor cells. FGFR1 is involved in the stimulation and proliferation of endothelial cells and vascularization by FGFs, particularly bFGF and aFGF. FGFs also promote the formation of hematopoietic progenitor cells in early development, which requires the FGFR1 as well.^7,8 In line with this, chromosomal translocation involving FGFR1 has been observed in patients with stem-cell myeloproliferative disease, probably caused by constitutive activation of the FGFR1 gene.⁹

See page 944

It has long been anticipated that hematopoietic progenitor cells and endothelial progenitor cells derive from a common cell type, the hemangioblast.¹⁰ Studies on mouse embryos have shown that such hemangioblast cells indeed exist. These cells develop in the primitive streak of the embryo and migrate to the yolk sac, where . . . [Full Text of this Article]

Related Article:

Fibroblast Growth Factor Receptor-1 Expression Is Required for Hematopoietic but not Endothelial Cell Development

Peetra Ulrica Magnusson, Roberto Ronca, Patrizia Dell’Era, Pia Carlstedt, Lars Jakobsson, Juha Partanen, Anna Dimberg, and Lena Claesson-Welsh
Arterioscler Thromb Vasc Biol 2005 25: 944-949. [Abstract] [Full Text] [PDF]