Role of NFkappaB in toll-like receptor 9-mediated matrix metalloproteinase-9 expression
Journal of the Korean Association of Oral and Maxillofacial Surgeons
;
: 636-642, 2007.
Artículo
en Coreano
| WPRIM
| ID: wpr-23649
ABSTRACT
BACKGROUND:
CpG DNA plays an important role in immune cell function. This study examined whether the temporal control of toll-like receptor (TLR)9 by CpG DNA can regulate the expression of matrix metalloproteinase-9 (MMP-9). MeETHODS AND MATERIALS Macrophages were cultured in the presence of 10percent FBS. For the various MMP genes analysis, RT-PCR and real-time PCR were performed. In addition, zymography assay performed for the MMP activity. The phosphorylation assay did for the ERK1/2 and NFkappaB activation, and luciferase promoter assay was for the NFkappaB activity.RESULTS:
CpG DNA induced the mRNA expression of MMP-2, MMP-9, and MMP-13, but not of MMP-7, MMP-8, and MMP-12, in a time-dependent manner. Especially, the mRNA expression of MMP-9 was strongly induced by CpG DNA using real-time RT-PCR. The TLR9 inhibitor, chloroquine, suppressed CpG DNA-induced MMP-9 expression and its activity. Moreover, CpG DNA induced the phosphorylation of ERK and the inhibition of ERK by U0126 suppressed CpG DNA-induced MMP-9 expression and its activity. CpG DNA stimulated IkappaB-alpha degradation and luciferase activity. In addition, pretreatment of SN-50, the inhibitor of NFkappaB, strongly blocked the CpG DNA-induced MMP-9 expression and activity.CONCLUSION:
These observations suggest that CpG DNA may play important roles in the activation of macrophages by regulating the production of MMP-9 via the sequential TLR9-ERK-NFkappaB signaling pathway.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fosforilación
/
ADN
/
ARN Mensajero
/
Cloroquina
/
Metaloproteinasa 9 de la Matriz
/
Receptores Toll-Like
/
Reacción en Cadena en Tiempo Real de la Polimerasa
/
Luciferasas
/
Macrófagos
Idioma:
Coreano
Revista:
Journal of the Korean Association of Oral and Maxillofacial Surgeons
Año:
2007
Tipo del documento:
Artículo
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