Double-Stranded RNA Induces MMP-9 Gene Expression in HaCaT Keratinocytes by Tumor Necrosis Factor-α.
Viral double-stranded RNA (dsRNA) and its synthetic analog poly (I:C) are recognized via multiple pathways and induce the expression of genes related to inflammation. In the present study, we demonstrate that poly (I:C) specifically induced the expression of matrix metallo¬proteinase-9 (MMP-9) in HaCaT keratinocytes. Studies using specific pharmacological inhibitors revealed the involvement of NF-κB, p38 MAPK, and PI-3K signal transduction pathways in poly (I:C)-induced MMP-9 gene expression. MMP-9 gene induction was sensitive toward treatment with the macrolide antibiotic bafilomycin A1, a vacuolar H(+)-ATPase inhibitor, and with the lysosomotropic agent chloroquine. However, cycloheximide treatment only partially blocked poly (I:C)-induced MMP-9 gene expression. Although HaCaT keratinocytes produce a number of cytokines and chemokines in response to poly (I:C), stimulation experiments revealed that exclusively TNFα strongly promoted MMP-9 gene expression. During the antiviral response MMP-9 expression may be of importance for the tissue injury phase.[1]References
- Double-Stranded RNA Induces MMP-9 Gene Expression in HaCaT Keratinocytes by Tumor Necrosis Factor-α. Voss, A., Gescher, K., Hensel, A., Nacken, W., Kerkhoff, C. Inflamm. Allergy. Drug. Targets (2011) [Pubmed]
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