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lncRNA‐CIR regulates cell apoptosis of chondrocytes in osteoarthritis
Author(s) -
Lu Zekai,
Luo Min,
Huang Yongpan
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27997
Subject(s) - gene knockdown , downregulation and upregulation , apoptosis , chondrocyte , dapi , microbiology and biotechnology , oxidative stress , chemistry , western blot , small interfering rna , cancer research , biology , cartilage , transfection , biochemistry , anatomy , gene
Background and Objectives Osteoarthritis (OA) is a complex chronic degenerative joint disease involving oxidative stress, inflammation, and apoptosis of chondrocytes. As decoys of micro RNAs, long non‐coding RNAs (lncRNAs) play important roles in various biological processes. This study was designed to investigate the interactions between lncRNA‐CIR, chondrocyte apoptosis, and the molecular mechanisms underlying OA. Methods Primary cultured chondrocytes were stressed using H 2 O 2 , IL‐1β, or TNF‐ɑ to simulate conditions found in OA. Quantitative real‐time PCR was performed to detect miR‐130a, lncRNA‐CIR, and Bim mRNA expression levels. Western blot analysis was used to detect Bim protein expression levels. Reactive oxygen species (ROS) levels were assayed by detecting the fluorescent signal of 2′,7′‐dichlorodihydrofluorescein diacetate (DCFH‐DA). Cell apoptosis was measured with combined staining of PI and DAPI. lncRNA‐CIR knockdown and miR‐130a over‐expression or inhibition were performed using small interfering RNAs, and miR‐130 mimics or inhibitors, respectively. Results lncRNA‐CIR is significantly upregulated in OA patients, accompanied by downregulation of miR‐130a and upregulation of Bim. Bio‐informatics analysis predicted miR‐130a as a target of both lncRNA‐CIR and Bim. While lncRNA‐CIR knockdown significantly increased the expression of Bim, miR‐130a significantly suppressed Bim expression, with accompanying increases of ROS level, inflammatory mediator release, cell apoptosis, and relative luciferase activity. Conclusions The present findings demonstrated that the lncRNA‐CIR/miR‐130a/Bim axis is involved in oxidative stress‐related apoptosis of chondrocytes in OA.