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Porphyromonas gingivalis-induced miR-132 regulates TNFα expression in THP-1 derived macrophages

BACKGROUND: Periodontitis is a chronic inflammatory disease induced by periodontopathogens such as Porphyromonas gingivalis (P. gingivalis). MicroRNAs (miRNAs) are small single-stranded noncoding RNAs that regulate gene expression at the level of translation. MiRNAs have been reported to be involved...

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Detalles Bibliográficos
Autores principales: Park, Mi Hee, Park, Eunjoo, Kim, Hyung-Joon, Na, Hee Sam, Chung, Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4912528/
https://www.ncbi.nlm.nih.gov/pubmed/27386246
http://dx.doi.org/10.1186/s40064-016-2363-6
Descripción
Sumario:BACKGROUND: Periodontitis is a chronic inflammatory disease induced by periodontopathogens such as Porphyromonas gingivalis (P. gingivalis). MicroRNAs (miRNAs) are small single-stranded noncoding RNAs that regulate gene expression at the level of translation. MiRNAs have been reported to be involved in inflammatory processes. In this study, we examined the effects of P. gingivalis-induced inflammatory miRNAs expression on TNFα production in THP-1 derived macrophages. RESULTS: Porphyromonas gingivalis induced the expression of miR-132. P. gingivalis-induced miR-132 expression was significantly inhibited by TLR2/4 knock-down and NF-κB inhibitor. Additionally, miR-132 antagomir strongly repressed production of TNFα. The expression of NFE2L2 and NFAT5, the putative target genes of miR-132 involved in regulation of TNFα, decreased in response to P. gingivalis. Furthermore, miR-132 antagomir rescued P. gingivalis-induced suppression of NFE2L2 and NFAT5. CONCLUSIONS: These results suggest that the induction of miR-132 by P. gingivalis can modulate the pathogenesis of periodontitis induced via regulatory expression of TNFα.