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ABSTRACT
Background
Osteoarthritis (OA) is a common degenerative joint disease in the elderly. Increasing evidence suggested that long non-coding RNAs (lncRNAs) played vital roles in OA progression. This study aimed to explore the role and mechanism of lncRNA small nucleolar RNA host gene 5 (SNHG5) in OA development.
Methods
Chondrocytes were stimulated with interleukin-1β (IL-1β) in vitro. The levels of SNHG5, miR-10a-5p, and H3 histone family 3B (H3F3B) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis was tested by flow cytometry. The levels of apoptosis-related and cartilage-related markers were detected by western blot. The interaction among SNHG5, miR-10a-5p, and H3F3B was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
Results
SNHG5 and H3F3B were downregulated, while miR-10a-5p was upregulated in OA cartilage tissues. Knockdown of SNHG5 enhanced IL-1β-induced apoptosis in chondrocytes. Rescue experiments verified that SNHG5 hindered apoptosis in IL-1β-stimulated chondrocytes by sponging miR-10a-5p. Moreover, H3F3B was a target of miR-10a-5p, and miR-10a-5p promoted IL-1β-induced chondrocyte apoptosis by regulating H3F3B. In addition, SNHG5 regulated H3F3B expression via sponging miR-10a-5p in IL-1β-treated chondrocytes.
Conclusion
SNHG5 suppressed chondrocytes apoptosis in OA by regulating the miR-10a-5p/H3F3B axis, which provided a promising biomarker for OA treatment.
Disclosure statement
No potential conflict of interest was reported by the author(s).