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Int. J. Mol. Sci. 2019, 20(4), 809; https://doi.org/10.3390/ijms20040809

MicroRNA-766-3p Contributes to Anti-Inflammatory Responses through the Indirect Inhibition of NF-κB Signaling

1
Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan
2
Department of Internal Medicine and Rheumatology, School of Medicine, Juntendo University, Tokyo 113-8421, Japan
3
Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan
*
Author to whom correspondence should be addressed.
Present Address: Department of Pharmaceutical Sciences, Musashino University, Tokyo 202-8585, Japan.
Present Address: Department of Internal Medicine and Rheumatology, Juntendo University Shizuoka Hospital, Shizuoka 410-2295, Japan.
Received: 11 January 2019 / Revised: 7 February 2019 / Accepted: 11 February 2019 / Published: 14 February 2019
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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Abstract

MicroRNA (miRNA) is small RNA of 20 to 22 nucleotides in length and is stably present in plasma. Regulating the expression of miRNA taken into cells has been suggested as a general therapeutic approach. We identified the novel anti-inflammatory miRNA hsa-miR-766-3p and investigated its biological function in human rheumatoid arthritis (RA) fibroblast-like synoviocyte MH7A cells. To verify the function of the miRNA present in the plasma of RA patients, we performed a comprehensive analysis of the miRNA expression during abatacept treatment and identified eight miRNAs with significantly altered expression levels. Among these eight miRNAs, miR-766-3p was found to have a clear function. The expression of inflammatory genes in response to inflammatory stimuli was suppressed in MH7A transduced with miR-766-3p. We showed that miR-766-3p indirectly reduced the activation of NF-κB and clarified that this mechanism was partially involved in the reduction of the mineralocorticoid receptor expression. In addition, the inflammatory responses were suppressed in other types of cells. These results indicate the novel function of miR-766-3p, findings that may aid in the development of therapies to suppress inflammation, not only in RA but also in other diseases. View Full-Text
Keywords: microRNA (miRNA); tumor necrosis factor-α (TNF-α); interleukin(IL)-1β; inflammation; nuclear factor-κB (NF-κB); rheumatoid arthritis (RA); abatacept; mineralocorticoid receptor microRNA (miRNA); tumor necrosis factor-α (TNF-α); interleukin(IL)-1β; inflammation; nuclear factor-κB (NF-κB); rheumatoid arthritis (RA); abatacept; mineralocorticoid receptor
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Hayakawa, K.; Kawasaki, M.; Hirai, T.; Yoshida, Y.; Tsushima, H.; Fujishiro, M.; Ikeda, K.; Morimoto, S.; Takamori, K.; Sekigawa, I. MicroRNA-766-3p Contributes to Anti-Inflammatory Responses through the Indirect Inhibition of NF-κB Signaling. Int. J. Mol. Sci. 2019, 20, 809.

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