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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

 Yeon Jeong Choi  ;  Charm Kim  ;  Eun Woo Choi  ;  Seung Hun Lee  ;  Min Kyung Chae  ;  Hyung Oh Jun  ;  Bo-Yeon Kim  ;  Jin Sook Yoon  ;  Sun Young Jang 
 PLOS ONE, Vol.17(8) : e0270416, 2022-08 
Journal Title
Issue Date
Anti-Inflammatory Agents / pharmacology ; Cells, Cultured ; Fibroblasts / metabolism ; Graves Ophthalmopathy* / pathology ; Humans ; Inflammation / pathology ; Interleukin-2 / metabolism ; Interleukin-6 / metabolism ; MicroRNAs* / metabolism ; Orbit / pathology ; Protein-Tyrosine Kinases ; T-Lymphocytes / metabolism ; Tumor Necrosis Factor-alpha / metabolism ; Tumor Necrosis Factor-alpha / pharmacology
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.
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1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Yoon, Jin Sook(윤진숙) ORCID logo https://orcid.org/0000-0002-8751-9467
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