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Article: miR-181d regulates human dendritic cell maturation through NF-κB pathway

TitlemiR-181d regulates human dendritic cell maturation through NF-κB pathway
Authors
Issue Date2017
Citation
Cell Proliferation, 2017, v. 50, n. 5, article no. e12358 How to Cite?
AbstractObjectives: MicroRNAs (miRNAs) are considered as the cellular regulators which post-transcriptionally modulate gene expression in diverse biological processes including cell development and immunity. In this study, we investigated functions of miR-181d in dendritic cells (DCs) maturation, and the underlying mechanisms were also explored. Materials and methods: Here we did the miRNA screening in human DCs in response to lipopolysaccharides (LPS) by quantitative real-time PCR (qRT-PCR). The expressions of DCs maturation markers were measured after miRNA mimics transfections. The pharmacological inhibitors of signalling pathways were applied to examine miR-181d effect on DCs maturation by Western blot. Luciferase assay and mixed lymphocyte reaction (MLR) were also performed to reveal the target gene of miR-181d and test the viability of T cells treated with miR-181d transfected DCs. Results: Overexpression of miR-181d per se is sufficient to promote DCs maturation, and up-regulate CD80 and CD83 expressions without LPS. Besides, we showed that miR-181d activated NF-κB pathway and also promoted the expression of pro-inflammatory cytokine IL12 and TNF-α. Inhibition of NF-κB pathway suppressed DCs maturation. Luciferase reporter assay and target gene knockdown assay indicated that miR-181d targets regulator cylindromatosis (CYLD), a primary negative regulator of NF-κB pathway. MLR assay showed that miR-181d-transfected DCs could promote T-cell proliferation than iDCs in vitro. Conclusion: Our study demonstrates that miR-181d is required for DCs maturation through the activation of NF-κB pathway by targeting CYLD.
Persistent Identifierhttp://hdl.handle.net/10722/325364
ISSN
2023 Impact Factor: 5.9
2023 SCImago Journal Rankings: 1.951
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSu, Xian Wei-
dc.contributor.authorLu, Gang-
dc.contributor.authorLeung, Chi Kwan-
dc.contributor.authorLiu, Qiang-
dc.contributor.authorLi, Yi-
dc.contributor.authorTsang, Kam Sze-
dc.contributor.authorZhao, Shi Dou-
dc.contributor.authorChan, Danny Tat Ming-
dc.contributor.authorKung, Hsiang Fu-
dc.contributor.authorPoon, Wai Sang-
dc.date.accessioned2023-02-27T07:31:53Z-
dc.date.available2023-02-27T07:31:53Z-
dc.date.issued2017-
dc.identifier.citationCell Proliferation, 2017, v. 50, n. 5, article no. e12358-
dc.identifier.issn0960-7722-
dc.identifier.urihttp://hdl.handle.net/10722/325364-
dc.description.abstractObjectives: MicroRNAs (miRNAs) are considered as the cellular regulators which post-transcriptionally modulate gene expression in diverse biological processes including cell development and immunity. In this study, we investigated functions of miR-181d in dendritic cells (DCs) maturation, and the underlying mechanisms were also explored. Materials and methods: Here we did the miRNA screening in human DCs in response to lipopolysaccharides (LPS) by quantitative real-time PCR (qRT-PCR). The expressions of DCs maturation markers were measured after miRNA mimics transfections. The pharmacological inhibitors of signalling pathways were applied to examine miR-181d effect on DCs maturation by Western blot. Luciferase assay and mixed lymphocyte reaction (MLR) were also performed to reveal the target gene of miR-181d and test the viability of T cells treated with miR-181d transfected DCs. Results: Overexpression of miR-181d per se is sufficient to promote DCs maturation, and up-regulate CD80 and CD83 expressions without LPS. Besides, we showed that miR-181d activated NF-κB pathway and also promoted the expression of pro-inflammatory cytokine IL12 and TNF-α. Inhibition of NF-κB pathway suppressed DCs maturation. Luciferase reporter assay and target gene knockdown assay indicated that miR-181d targets regulator cylindromatosis (CYLD), a primary negative regulator of NF-κB pathway. MLR assay showed that miR-181d-transfected DCs could promote T-cell proliferation than iDCs in vitro. Conclusion: Our study demonstrates that miR-181d is required for DCs maturation through the activation of NF-κB pathway by targeting CYLD.-
dc.languageeng-
dc.relation.ispartofCell Proliferation-
dc.titlemiR-181d regulates human dendritic cell maturation through NF-κB pathway-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/cpr.12358-
dc.identifier.pmid28731516-
dc.identifier.scopuseid_2-s2.0-85028750437-
dc.identifier.volume50-
dc.identifier.issue5-
dc.identifier.spagearticle no. e12358-
dc.identifier.epagearticle no. e12358-
dc.identifier.eissn1365-2184-
dc.identifier.isiWOS:000409197900008-

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