MicroRNA-766-3p Contributes to Anti-Inflammatory Responses through the Indirect Inhibition of NF-κB Signaling
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 fu...
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Published in | International journal of molecular sciences Vol. 20; no. 4; p. 809 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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14.02.2019
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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. |
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AbstractList | 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. [...]it did not promote inflammatory responses (Figure 2G), making it unlikely that intracellular miR-766-3p typically participates in anti-inflammatory mechanisms. [...]for miR-766-3p to exhibit an anti-inflammatory effect in MH7A cells, miRNA needs to be taken up from extracellular sources. 2.4. Besides NF-κB, AP-1—which regulates inflammatory processes—is another important transcription factor in inflammatory cytokine signaling [12]. [...]several reports have shown an association between MCR and inflammatory responses [14,15]. [...]we examined the association between MCR and NF-κB activation after TNF-α or IL-1β stimulation in MH7A cells. The cytokine-inducible CCL2 expression was dependent on NF-κB [16], whereas the constitutive expression of CCL2 was dependent on NF-κB and AP-1 [17]. [...]we examined the NF-κB activity using a reporter assay. |
Author | Ikeda, Keigo Sekigawa, Iwao Hayakawa, Kunihiro Hirai, Takuya Yoshida, Yuko Takamori, Kenji Tsushima, Hiroshi Fujishiro, Maki Kawasaki, Mikiko Morimoto, Shinji |
AuthorAffiliation | 2 Department of Internal Medicine and Rheumatology, School of Medicine, Juntendo University, Tokyo 113-8421, Japan 1 Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan; mikidx@nifty.com (M.K.); thirai@juntendo.ac.jp (T.H.); yyoshida@musashino-u.ac.jp (Y.Y.); htsushi@juntendo.ac.jp (H.T.); mfujishi@juntendo.ac.jp (M.F.); ktakamor@juntendo.ac.jp (K.T.); isekigawa@mva.biglobe.ne.jp (I.S.) 3 Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan; keigo@juntendo.ac.jp (K.I.); morimoto@juntendo.ac.jp (S.M.) |
AuthorAffiliation_xml | – name: 1 Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan; mikidx@nifty.com (M.K.); thirai@juntendo.ac.jp (T.H.); yyoshida@musashino-u.ac.jp (Y.Y.); htsushi@juntendo.ac.jp (H.T.); mfujishi@juntendo.ac.jp (M.F.); ktakamor@juntendo.ac.jp (K.T.); isekigawa@mva.biglobe.ne.jp (I.S.) – name: 3 Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan; keigo@juntendo.ac.jp (K.I.); morimoto@juntendo.ac.jp (S.M.) – name: 2 Department of Internal Medicine and Rheumatology, School of Medicine, Juntendo University, Tokyo 113-8421, Japan |
Author_xml | – sequence: 1 givenname: Kunihiro orcidid: 0000-0002-8053-746X surname: Hayakawa fullname: Hayakawa, Kunihiro email: khayaka@juntendo.ac.jp organization: Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan. khayaka@juntendo.ac.jp – sequence: 2 givenname: Mikiko surname: Kawasaki fullname: Kawasaki, Mikiko email: mikidx@nifty.com organization: Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan. mikidx@nifty.com – sequence: 3 givenname: Takuya surname: Hirai fullname: Hirai, Takuya email: thirai@juntendo.ac.jp, thirai@juntendo.ac.jp organization: Department of Internal Medicine and Rheumatology, School of Medicine, Juntendo University, Tokyo 113-8421, Japan. thirai@juntendo.ac.jp – sequence: 4 givenname: Yuko surname: Yoshida fullname: Yoshida, Yuko email: yyoshida@musashino-u.ac.jp organization: Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan. yyoshida@musashino-u.ac.jp – sequence: 5 givenname: Hiroshi surname: Tsushima fullname: Tsushima, Hiroshi email: htsushi@juntendo.ac.jp, htsushi@juntendo.ac.jp organization: Department of Internal Medicine and Rheumatology, School of Medicine, Juntendo University, Tokyo 113-8421, Japan. htsushi@juntendo.ac.jp – sequence: 6 givenname: Maki surname: Fujishiro fullname: Fujishiro, Maki email: mfujishi@juntendo.ac.jp organization: Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan. mfujishi@juntendo.ac.jp – sequence: 7 givenname: Keigo orcidid: 0000-0002-8032-7147 surname: Ikeda fullname: Ikeda, Keigo email: keigo@juntendo.ac.jp organization: Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan. keigo@juntendo.ac.jp – sequence: 8 givenname: Shinji surname: Morimoto fullname: Morimoto, Shinji email: morimoto@juntendo.ac.jp organization: Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan. morimoto@juntendo.ac.jp – sequence: 9 givenname: Kenji surname: Takamori fullname: Takamori, Kenji email: ktakamor@juntendo.ac.jp organization: Institute for Environment and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Chiba 279-0021, Japan. ktakamor@juntendo.ac.jp – sequence: 10 givenname: Iwao surname: Sekigawa fullname: Sekigawa, Iwao email: isekigawa@mva.biglobe.ne.jp, isekigawa@mva.biglobe.ne.jp organization: Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan. isekigawa@mva.biglobe.ne.jp |
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Keywords | microRNA (miRNA) inflammation interleukin(IL)-1β abatacept rheumatoid arthritis (RA) mineralocorticoid receptor nuclear factor-κB (NF-κB) tumor necrosis factor-α (TNF-α) |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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. |
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Snippet | 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... [...]it did not promote inflammatory responses (Figure 2G), making it unlikely that intracellular miR-766-3p typically participates in anti-inflammatory... |
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SubjectTerms | abatacept Activator protein 1 Cytokines Gene expression IL-1β Inflammation interleukin(IL)-1β microRNA (miRNA) MicroRNAs mineralocorticoid receptor miRNA Monocyte chemoattractant protein 1 NF-κB protein nuclear factor-κB (NF-κB) rheumatoid arthritis (RA) Signal transduction Transcription factors Tumor necrosis factor-TNF Tumor necrosis factor-α tumor necrosis factor-α (TNF-α) |
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Title | MicroRNA-766-3p Contributes to Anti-Inflammatory Responses through the Indirect Inhibition of NF-κB Signaling |
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