DICAM Inhibits Activation of Macrophage by Lipopolysaccharide
Journal of Rheumatic Diseases
;
: 196-205, 2012.
Article
Dans Coréen
| WPRIM
| ID: wpr-11345
ABSTRACT
OBJECTIVE:
DICAM, a dual Ig domain containing adhesion molecule, is involved in cell-cell adhesion through direct interaction with alphavbeta3 integrin. In our previous study showing the inhibitory role of DICAM in osteoclast differentiation, we found that DICAM also has a suppressive role in macrophage, the precursor cell of osteoclast. The role of DICAM in macrophage activation at the inflammatory milieu, however, remains obscure.METHODS:
Expression pattern of DICAM by inflammatory cytokines and lipopolysaccharide (LPS) was studied with RAW264.7, a murine macrophage cell line. To study the role of DICAM on macrophage activation, we stably transduced DICAM, or empty vector, into RAW264.7, and then compared the LPS-mediated activation such as spreading and TNF-alpha production.RESULTS:
DICAM was abundantly expressed in the synovial tissue of collagen-induced arthritis. When we assessed the expression of DICAM in RAW264.7 cells by mediators of inflammation, inflammatory cytokines, such as TNF-alpha, IL-1beta, and IFN-gamma, and M-CSF increased the expression of DICAM; however, LPS decreased. Functionally, DICAM that stably transduced-RAW264.7 cells showed attenuation of LPS-mediated macrophage activation including spreading and TNF-alpha production. DICAM decreased the phosphorylation of JNK MAP kinase by M-CSF and LPS stimulation, which was corroborated by a decrease in the expression of ITAM-associated receptors including Trem2, Pira1, and Oscar. Finally, a recombinant ectodomain of DICAM suppressed LPS-induced activation of RAW264.7 cells.CONCLUSION:
These results indicate that DICAM acts as a negative regulator of LPS-mediated macrophage activation.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Ostéoclastes
/
Phosphorylation
/
Phosphotransferases
/
Arthrite expérimentale
/
Monocytes
/
Lignée cellulaire
/
Cytokines
/
Facteur de stimulation des colonies de macrophages
/
Facteur de nécrose tumorale alpha
/
Médiateurs de l'inflammation
langue:
Coréen
Texte intégral:
Journal of Rheumatic Diseases
Année:
2012
Type:
Article
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