| Literature DB >> 28088550 |
Gyeoung-Jin Kang1, Hye-Ja Lee1, Hyun Jung Byun1, Eun Ji Kim1, Hyun Ji Kim1, Mi Kyung Park1, Chang-Hoon Lee2.
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-miR-522-3p-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.Entities:
Keywords: Antiresolution factor; HMGB1; Inflammation; PTGR1; Phagocytosis; miR-522-3p
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Year: 2017 PMID: 28088550 DOI: 10.1016/j.bbamcr.2017.01.006
Source DB: PubMed Journal: Biochim Biophys Acta Mol Cell Res ISSN: 0167-4889 Impact factor: 4.739