Open AccessCircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR ‐30a‐3p and promoting PON2
Author(s) -
Shang Jie,
Li Huizi,
Wu Biao,
Jiang Ning,
Wang Bin,
Wang Dawei,
Zhong Junlong,
Chen Yufeng,
Xu Xianghe,
Lu Huading
Publication year - 2022
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.13285
Subject(s) - chondrocyte , apoptosis , microbiology and biotechnology , western blot , cartilage , chemistry , intracellular , mitochondrion , osteoarthritis , biology , medicine , biochemistry , gene , anatomy , pathology , alternative medicine
Osteoarthritis (OA) is a common joint disease featured by the deterioration of articular cartilage and chondrocyte death. Emerging evidence has indicated that circular RNAs (circRNAs) play an essential role in OA progress. Here, we found that the expression of circHIPK3 was significantly decreased in human and mouse OA cartilage. Knocking down circHIPK3 increased apoptosis and intracellular ROS level in HC‐a chondrocytes. We performed proteomic studies and identified that circHIPK3 regulated chondrocyte apoptosis through the mitochondrial pathway. Results of JC‐1 staining and western blot further confirmed that mitochondrial outer membrane permeabilization was promoted in HC‐a chondrocytes transfected by circHIPK3 siRNA. In terms of mechanism, we showed that PON2 functioned as a potential target of circHIPK3 to regulate chondrocyte apoptosis. Moreover, we revealed that circHIPK3 interacted with miR‐30a‐3p to regulate PON2 expression in chondrocytes. Taken together, our findings suggested that circHIPK3 regulated chondrocyte apoptosis by mitochondrial pathway, and targeting the circHIPK3/miR‐30a‐3p/PON2 axis might be a potential strategy for OA treatment.