Housen Jiang1, Hui Pang2, Peigang Wu3, Zhenhao Cao1, Zhong Li1, Xuedong Yang1. 1. Department of Hand and Foot Bone Surgery, Weifang People's Hospital, Weifang, Shandong, China. 2. Department of Hand and Foot Bone Surgery, Binzhou People's Hospital, Binzhou, Shandong, China. 3. Weifang Medical University, Weifang, Shandong, China.
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.
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.