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Vascular expression of the chemokine CX3CL1 promotes osteoclast recruitment and exacerbates bone resorption in an irradiated murine model

Authors
  • Han, Ki Hoon
  • Ryu, Jae Won
  • Lim, Kyung-Eun
  • Lee, Soo-Han
  • Kim, Yuna
  • Hwang, Chang Sun
  • Choi, Je-Yong
  • Han, Ki Ok1, 2, 3, 4, 5, 2, 6, 7, 8, 9, 2, 3, 4, 10, 2, 11, 10, 12
  • 1 Department of Cardiology
  • 2 School of Medicine
  • 3 University of Ulsan
  • 4 Asan Medical Center
  • 5 Department of Biochemistry and Cell Biology
  • 6 WCU Program
  • 7 Skeletal Diseases Genome Research Center
  • 8 Kyungpook National University
  • 9 Department of Cardiology and Pharmacology
  • 10 Department of Endocrinology and Metabolism
  • 11 Kwandong University
  • 12 G-SAM Medical Center
Type
Published Article
Journal
Bone
Publisher
Elsevier
Publication Date
Jan 01, 2014
Accepted Date
Dec 27, 2013
Volume
61
Pages
91–101
Identifiers
DOI: 10.1016/j.bone.2013.12.032
Source
Elsevier
Keywords
License
Unknown

Abstract

•Irradiation strongly upregulates CX3CL1 (fractalkine) production in the vascular endothelium.•CX3CL1 facilitates the recruitment of circulating CX3CR1 (receptor for CX3CL1)-expressing osteoclast precursor monocytes to irradiated bones.•CX3CL1 induces the expression of CXCL2 and CXCL12 through the HIF-1α/VEGF-A pathway.•Radiation-induced osteoclastogenesis and bone loss are attenuated by antibody neutralization of CX3CL1 or genetic knocking out of CX3CR1.

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