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MicroRNA-155 acts as an anti-inflammatory factor in orbital fibroblasts from Graves' orbitopathy by repressing interleukin-2-inducible T-cell kinase
DC Field | Value | Language |
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dc.contributor.author | 윤진숙 | - |
dc.date.accessioned | 2023-03-03T02:54:51Z | - |
dc.date.available | 2023-03-03T02:54:51Z | - |
dc.date.issued | 2022-08 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/192930 | - |
dc.description.abstract | To investigate the role of microRNA (miR)-155 in inflammation in an in-vitro model of Graves' orbitopathy (GO). The expression levels of miR-155 were compared between GO and non-GO orbital tissues. The effects of inflammatory stimulation of interleukin (IL)-1β and tumour necrosis factor alpha (TNF-α) on miR-155 expression on GO and non-GO orbital fibroblasts (OFs) were investigated. The effects of miR-155 mimics and inhibitors of inflammatory proteins and IL-2-inducible T-cell kinase (ITK) expression were examined, along with those related to the knockdown of ITK with siITK transfection on inflammatory proteins. We also examined how ITK inhibitors affect miR-155 expression in GO and non-GO OFs. The expression levels of miR-155 were higher in GO orbital tissues than in non-GO tissue. The overexpression of miR-155 was induced by IL-1β and TNF-α in OFs from GO and non-GO patients. IL-1β-induced IL-6 (ICAM1) protein production was significantly reduced (increased) by miR-155 mimics and inhibitors. The mRNA and protein levels of ITK were downregulated by overexpressed miR-155 via miR-155 mimics. Knockdown of ITK via siITK transfection induced a decrease in the expression levels of ITK, IL-17, IL-6, IL-1β, and TNF-α protein. The expression of miR-155 was significantly downregulated by treatment with ITK inhibitors and Bruton's tyrosine kinase (BTK)/ITK dual inhibitors in a time-dependent manner. Our results indicated a potential relationship between miR-155 and ITK in the context of GO OFs. The overexpression of miR-155 repressed ITK expression and relieved inflammation. Thus, miR-155 appears to have anti-inflammatory effects in GO OFs. This discovery provides a new concept for developing GO treatment therapeutics. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | Public Library of Science | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Anti-Inflammatory Agents / pharmacology | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | Fibroblasts / metabolism | - |
dc.subject.MESH | Graves Ophthalmopathy* / pathology | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Inflammation / pathology | - |
dc.subject.MESH | Interleukin-2 / metabolism | - |
dc.subject.MESH | Interleukin-6 / metabolism | - |
dc.subject.MESH | MicroRNAs* / metabolism | - |
dc.subject.MESH | Orbit / pathology | - |
dc.subject.MESH | Protein-Tyrosine Kinases | - |
dc.subject.MESH | T-Lymphocytes / metabolism | - |
dc.subject.MESH | Tumor Necrosis Factor-alpha / metabolism | - |
dc.subject.MESH | Tumor Necrosis Factor-alpha / pharmacology | - |
dc.title | MicroRNA-155 acts as an anti-inflammatory factor in orbital fibroblasts from Graves' orbitopathy by repressing interleukin-2-inducible T-cell kinase | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Ophthalmology (안과학교실) | - |
dc.contributor.googleauthor | Yeon Jeong Choi | - |
dc.contributor.googleauthor | Charm Kim | - |
dc.contributor.googleauthor | Eun Woo Choi | - |
dc.contributor.googleauthor | Seung Hun Lee | - |
dc.contributor.googleauthor | Min Kyung Chae | - |
dc.contributor.googleauthor | Hyung Oh Jun | - |
dc.contributor.googleauthor | Bo-Yeon Kim | - |
dc.contributor.googleauthor | Jin Sook Yoon | - |
dc.contributor.googleauthor | Sun Young Jang | - |
dc.identifier.doi | 10.1371/journal.pone.0270416 | - |
dc.contributor.localId | A02611 | - |
dc.relation.journalcode | J02540 | - |
dc.identifier.eissn | 1932-6203 | - |
dc.identifier.pmid | 35980936 | - |
dc.contributor.alternativeName | Yoon, Jin Sook | - |
dc.contributor.affiliatedAuthor | 윤진숙 | - |
dc.citation.volume | 17 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | e0270416 | - |
dc.identifier.bibliographicCitation | PLOS ONE, Vol.17(8) : e0270416, 2022-08 | - |
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