Abstract
A number of chemokines induce angiogenesis and endothelial cells express several chemokine receptors. To date, only a limited number of CC chemokines for CCR1 have been reported to induce angiogenic responses. We investigated the ability of CCL23 (also known as MPIF-1, MIP-3, or CKβ8) to promote angiogenesis, which induces chemotaxis of immune cells through CCR1. CCL23 promoted the chemotactic migration and differentiation of endothelial cells, and neovascularization in the chick chorioallantoic membrane. An N-terminal truncated form of CCL23 was at least 100-fold more potent than its intact form and was comparable to that of FGF in the angiogenic activities. Treatment with either pertussis toxin or anti-CCR1 antibody completely inhibited the CCL23-induced endothelial cell migration, indicating that endothelial cell migration was mediated through CCR1. CCL23 didn't promote the migration of HT1080 human fibrosarcoma cells that did not express CCR1. Our results suggest a role of CCL23 in angiogenesis in vitro as well as in vivo.
Original language | English |
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Pages (from-to) | 254-263 |
Number of pages | 10 |
Journal | Cytokine |
Volume | 30 |
Issue number | 5 |
DOIs | |
Publication status | Published - 2005 Jun 7 |
Externally published | Yes |
Bibliographical note
Funding Information:This study was supported by Immunomodulation Research Center grant from KOSEF and a grant from Kyung Hee University (to J. K.) and by a grant from the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (0320380-2 to Y. S. G.).
Keywords
- Angiogenesis
- CCL23
- CCR1
- CKβ8
- Chemokine
- Endothelial cells
- MIP-3
- MPIF-1
ASJC Scopus subject areas
- Molecular Biology
- Hematology
- Biochemistry
- Immunology and Allergy
- Immunology