Novel involvement of miR-522-3p in high-mobility group box 1-induced prostaglandin reductase 1 expression and reduction of phagocytosisopen access
- Authors
- Kang, Gyeoung-Jin; Lee, Hye-Ja; Byun, Hyun Jung; Kim, Eun Ji; Kim, Hyun Ji; Park, Mi Kyung; Lee, Chang-Hoon
- Issue Date
- Apr-2017
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Inflammation; HMGBI PTGR1; miR-522-3p; Phagocytosis; Antiresolution factor
- Citation
- BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, v.1864, no.4, pp 625 - 633
- Pages
- 9
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
- Volume
- 1864
- Number
- 4
- Start Page
- 625
- End Page
- 633
- URI
- https://scholarworks.dongguk.edu/handle/sw.dongguk/14791
- DOI
- 10.1016/j.bbamcr.2017.01.006
- ISSN
- 0167-4889
1879-2596
- Abstract
- Resolution of inflammation is important for physiological homeostasis. Chronic inflammatory diseases may be caused by abnormal resolution of inflammation. However, what causes a failure of inflammatory resolution is unclear. Here we investigated the involvement of high mobility group box 1 (HMGB1) protein in the control of inflammatory resolution as an 'anti -resolution factor'. We first confirmed the increased expression of HMGB1 and prostaglandin reductase 1 (PTGR1) in inflammatory conditions and HMGB1-mediated regulation of the expression of PTGR1. The inhibition of phagocytosis by HMGB1 was abrogated by PTGR1 silencing. PTGR1 was a direct target of miR522-3p and its expression was regulated by miRNA-522-3p inhibitor or mimic. Finally, miR-522-3p had an important role in the regulation of PTGR1 expression by HMGB1. The data indicates that HMGB1-miR522-3p-PTGR1 axis may be involved in the abnormal resolution of inflammation and suggests that this mechanism might be a target for modulation of chronic inflammatory disorder. (C) 2017 Elsevier B.V. All rights reserved.
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