LncRNA DILC participates in rheumatoid arthritis by inducing apoptosis of fibroblast-like synoviocytes and down-regulating IL-6

IL-6 produced by human fibroblast-like synoviocytes (HFLS) promotes rheumatoid arthritis (RA), while lncRNA DILC regulates liver cancer stem cells by inhibiting IL-6. Therefore, lncRNA DILC may participate in RA. In the present study, we found that plasma lncRNA DILC was down-regulated, while IL-6 w...

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Detalles Bibliográficos
Autores principales: Wang, Guan, Tang, Lian, Zhang, Xihai, Li, Yao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Research Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499449/
https://www.ncbi.nlm.nih.gov/pubmed/30944206
http://dx.doi.org/10.1042/BSR20182374
Descripción
Sumario:IL-6 produced by human fibroblast-like synoviocytes (HFLS) promotes rheumatoid arthritis (RA), while lncRNA DILC regulates liver cancer stem cells by inhibiting IL-6. Therefore, lncRNA DILC may participate in RA. In the present study, we found that plasma lncRNA DILC was down-regulated, while IL-6 was up-regulated in RA patients than in healthy controls. Plasma levels of lncRNA DILC and IL-6 were significantly and inversely correlated only in RA patients. Overexpression of lncRNA DILC resulted in promoted apoptosis of HFLS isolated from RA patients, while lncRNA DILC siRNA silencing played an opposite role. In addition, overexpression of lncRNA DILC also resulted in inhibited IL-6 expression in HFLS isolated from RA patients. Therefore, lncRNA DILC may participate in RA by inducing apoptosis of HFLS and down-regulating IL-6.

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