Toll-like receptor 9-¸Å°³¿¡ ÀÇÇÑ matrix metalloproteinase-9 ¹ßÇö¿¡¼ NF¥êBÀÇ ¿ªÇÒ
ROLE OF NF¥êB IN TOLL-LIKE RECEPTOR 9-MEDIATED MATRIX METALLOPROTEINASE-9 EXPRESSION
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ÀÌ»óÈÆ ( Lee Sang-Hoon ) - ¿µ³²´ëÇб³ ÀÇ°ú´ëÇÐ Ä¡°úÇб³½Ç
Áøº´·Î ( Chin Byung-Rho ) - ¿µ³²´ëÇб³ ÀÇ°ú´ëÇÐ Ä¡°úÇб³½Ç
¹é¼®È¯ ( Baek Suk-Hwan ) - ¿µ³²´ëÇб³ ÀÇ°ú´ëÇÐ »ýÈÇкÐÀÚ»ý¹°Çб³½Ç
KMID : 0355620070330060636
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).
Materials and Methods: Macrophages were cultured in the presence of 10% 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 NF¥êB activation, and luciferase promoter assay was for the NF¥êB 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 I¥êB-¥ádegradation and luciferase activity. In addition, pretreatment of SN-50, the inhibitor of NF¥êB, 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-NF¥êB signaling pathway.
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Toll-like receptor;Matrix metalloproteinase;NF¥êB
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