CXCL16 is a novel angiogenic factor for human umbilical vein endothelial cells

CXCL16 is a unique chemokine with characteristics as a receptor for phosphatidylserine and oxidized low density lipoproteins in macrophages, and is involved in the accumulation of cellular cholesterol during atherosclerotic lesion development. In this study, we report a new function of CXCL16 as a n...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-06, Vol.331 (4), p.1295-1300
Main Authors: Zhuge, Xin, Murayama, Toshinori, Arai, Hidenori, Yamauchi, Ryoko, Tanaka, Makoto, Shimaoka, Takeshi, Yonehara, Shin, Kume, Noriaki, Yokode, Masayuki, Kita, Toru
Format: Article
Language:English
Subjects:
Angiogenesis
Cell Movement - physiology
Cell Proliferation
Cells, Cultured
Chemokine CXCL16
Chemokines, CXC - physiology
CXCL16
Endothelial cell
Endothelium, Vascular - cytology
Humans
Membrane Proteins - physiology
Neovascularization, Physiologic - physiology
Receptors, Immunologic - physiology
Receptors, Scavenger
Umbilical Veins - cytology
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Summary:CXCL16 is a unique chemokine with characteristics as a receptor for phosphatidylserine and oxidized low density lipoproteins in macrophages, and is involved in the accumulation of cellular cholesterol during atherosclerotic lesion development. In this study, we report a new function of CXCL16 as a novel angiogenic factor in human umbilical vein endothelial cells (HUVEC). CXCL16 stimulated proliferation and chemotaxis of HUVEC in a dose-dependent manner, reaching a maximum at 1 nM. CXCL16 also significantly induced tube formation of HUVEC on Matrigel. Further, exposure of HUVEC to CXCL16 led to a time- and dose-dependent activation of mitogen-activated protein kinase (ERK1/2), which was completely inhibited by a mitogen-activated protein kinase kinase inhibitor, PD98059. Proliferation and tube formation in response to CXCL16 were also blocked by the pretreatment with PD98059, but not CXCL16-induced chemotaxis. Thus, our data indicate that CXCL16 may act as a novel angiogenic factor for HUVEC and that ERK is involved as an important signaling molecule to mediate its angiogenic effects.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.03.200