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Long noncoding RNA LINC00662‐miR‐15b‐5p mediated GPR120 dysregulation contributes to osteoarthritis
Author(s) -
Lu Ming,
Zhou Enliang
Publication year - 2020
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12875
Subject(s) - microrna , apoptosis , receptor , signal transduction , cancer research , gpr120 , untranslated region , osteoarthritis , microbiology and biotechnology , biology , tumor necrosis factor alpha , rna , g protein coupled receptor , medicine , immunology , gene , pathology , biochemistry , alternative medicine
Previous studies demonstrated that dysregulation of G protein‐coupled receptor 120 (GPR120) plays a protective role in osteoarthritis (OA). However, the mechanism underlying how GPR120 is downregulated remains largely unknown. In the present study, we evaluated whether GPR120 is regulated by microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). Our results show that GPR120 was negatively regulated by miR‐15b‐5p through targeting 3′ untranslated region (3′UTR), and that miR‐15b‐5p was negatively regulated by LINC00662. Further luciferase assay shows that LINC00662‐miR‐15b‐5p signaling pathway contributed the regulation of GPR120 expression. Functionally, the decreased of LINC00662 caused increased miR‐15b‐5p, thereby leading to decreased GPR120. The decreased GPR120 then contributes to increased expression of inflammatory factors including tumor necrosis factor α (TNF‐α), interleukin (IL)‐6 and IL‐8, cell apoptosis, and decreased apoptosis‐related protein levels including cleaved caspase‐3, cleaved caspase‐9, and Bax in cultured rat chondrocytes. In summary, the present study shows that LINC00662‐miR‐15b‐5p signaling pathway is involved in the regulation of GPR120, thereby contributing to arthritis.