Chemokine Lkn-1/CCL15 enhances matrix metalloproteinase-9 release from human macrophages and macrophage-derived foam cells.
- Author:
Sang Hee KWON
1
;
Seong A JU
;
Ji Hye KANG
;
Chu Sook KIM
;
Hyeon Mi YOO
;
Rina YU
Author Information
- Publication Type:Brief Communication
- Keywords: Chemokine; Lkn-1/CCL15; MMP-9; foam cell; atherosclerosis
- MeSH: Atherosclerosis; Chemokines; Foam Cells; Gelatin; Humans; Leukocytes; Lipoproteins, LDL; Macrophages; Matrix Metalloproteinase 9; Matrix Metalloproteinases; Monocytes; Phorbols; Rupture; Tetradecanoylphorbol Acetate
- From:Nutrition Research and Practice 2008;2(2):134-137
- CountryRepublic of Korea
- Language:English
- Abstract: Atherosclerosis is characterized by a chronic inflammatory disease, and chemokines play an important role in both initiation and progression of atherosclerosis development. Leukotactin-1 (Lkn-1/CCL15), a new member of the human CC chemokine family, is a potent chemoattractant for leukocytes. Our previous study has demonstrated that Lkn-1/CCL15 plays a role in the initiation of atherosclerosis, however, little is currently known whether Lkn-1/CCL15 is associated with the progression of atherosclerosis. Matrix metalloproteinases (MMPs) in human coronary atherosclerotic lesions play a crucial role in the progression of atherosclerosis by altering the vulnerability of plaque rupture. In the present study, we examined whether Lkn-1/CCL15 modulates MMP-9 release, which is a prevalent form expressed by activated macrophages and foam cells. Human THP-1 monocytic cells and/or human peripheral blood monocytes (PBMC) were treated with phorbol myristate acetate to induce their differentiation into macrophages. Foam cells were prepared by the treatment of THP-1 macrophages with human oxidized LDL. The macrophages and foam cells were treated with Lkn-1/CCL15, and the levels of MMP-9 release were measured by Gelatin Zymography. Lkn-1/CCL15 significantly enhanced the levels of MMP-9 protein secretion from THP-1 monocytic cells-derived macrophages, human PBMC-derived macrophages, as well as macrophage-derived foam cell in a dose dependent manner. Our data suggest that the action of Lkn-1/CCL15 on macrophages and foam cells to release MMP-9 may contribute to plaque destabilization in the progression of atherosclerosis.
