Long non-coding RNA SNHG15 is a competing endogenous RNA of miR-141-3p that prevents osteoarthritis progression by upregulating BCL2L13 expression

Xing, Zhou; Huang, Chao-ran; Pan, Sheng; Pang, Yong; Chen, Ye-Shuai; Zha, Guo-Chun; Guo, Kaijin; Zheng, Xin

doi:10.1016/j.intimp.2020.106425

Cited by 31 publications

(14 citation statements)

References 31 publications

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“…Increasing evidence suggests that lncRNA SNHG15 can mediate many human cancers by sponging several miRNAs [ 9 – 11 ]. A recent study has reported that SNHG15 is downregulated in OA cartilage tissue and IL-1β-induced chondrocytes [ 12 ]. Furthermore, inhibition of SNHG15 can reduce chondrocyte apoptosis and ECM degradation and ameliorate articular cartilage damage, indicating that SNHG15 is involved in the progression of OA.…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 15 (SNHG15) Alleviates Osteoarthritis Progression by Regulation of Extracellular Matrix Homeostasis

Chen

Guo

et al. 2020

Med Sci Monit

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Background Growing evidence suggests that long non-coding RNAs (lncRNAs), as decoys of microRNAs (miRNAs), are involved in osteoarthritis (OA) progression, but the potential mechanism of lncRNA SNHG15 in OA remains unknown. Thus, the present study explored the molecular mechanism of SNHG15 in OA progression. Material/Methods OA chondrocytes were created by 20 ng/ml IL-1β stimulation, and the experimental OA model was created by destabilization of the medial meniscus (DMM) surgery. Cartilage histomorphology was observed by safranin and fast green double dyeing. The relationships between SNHG15 and miR-7, KLF4, and miR-7 were determined by dual-luciferase assay or RNA immunoprecipitation (RIP). Immunofluorescence was used to detect the expressions of Ki67, collagen II, and Aggrecan. Moreover, SNHG15, miR-7, KLF4, MMP3, ADAMTS5, COL2A1, Aggrecan, and β-catenin expressions were assessed by qRT-PCR or Western blot. The methylation status of SNHG15 promoter was evaluated by MS-PCR. Results Underexpression of KLF4 and SHNG15 and overexpression of miR-7 were found in human OA knee cartilage tissues and IL-1β-stimulated OA chondrocytes. SHNG15 overexpression significantly inhibited ECM degradation and promoted chondrocyte formation of OA chondrocytes. Furthermore, SNHG15 regulated KLF4 expression by sponging miR-7. Further analysis found that SNHG15 significantly inhibited β-catenin in OA chondrocytes. SNHG15 had a higher level of methylation in human OA tissues than in normal cartilage tissues. Conclusions Our results revealed that SNHG15 alleviated OA progression by regulating ECM homeostasis, which provides a promising target for OA therapy.

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Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 15 (SNHG15) Alleviates Osteoarthritis Progression by Regulation of Extracellular Matrix Homeostasis

Chen

Guo

et al. 2020

Med Sci Monit

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“…IL‐1β is a small molecule that modulates inflammation and plays a vital role in OA occurrence 24 . In light of its effects, IL‐1β has been widely used to mimic OA in studies in vitro 25,26 . Therefore, we investigated IL‐1β‐stimulated chondrocytes to explore the in‐depth mechanism of circADAMTS6 in vitro .…”

Section: Discussionmentioning

confidence: 99%

“…24 In light of its effects, IL-1β has been widely used to mimic OA in studies in vitro. 25,26 Therefore, we investigated IL-1β-stimulated chondrocytes to explore the in-depth mechanism of circADAMTS6 in vitro. We demonstrated that IL-1β significantly induced apoptosis of chondrocytes using annexin-V-FITC, which indicated that the OA cell model was established successfully.…”

Section: Discussionmentioning

confidence: 99%

CircADAMTS6/miR‐431‐5p axis regulate interleukin‐1β induced chondrocyte apoptosis

Wang

et al. 2021

The Journal of Gene Medicine

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Background: Growing evidence suggests that circular RNAs (circRNAs) are involved in the development of osteoarthritis (OA). The present study aimed to explore the CircADAMTS6/miR-431-5p axis with respect to regulating interleukin-1β (IL-1β) induced chondrocyte apoptosis. Methods: We first evaluated the differentially expressed circRNAs between normal chondrocytes and interleukin (IL)-1β-stimulated chondrocytes. Then, bioinformatic analysis was performed to identify the role and function of circADAMTS6. Small interfering RNA-expressing or overexpressing circADAMTS6 lentiviral vectors were used for transduction of chondrocytes. Annexin-V-fluorescein isothiocyanate (FITC) double staining was performed to measure the apoptotic rate of the chondrocytes in each group. Finally, a dual luciferase reporter assay was performed to identify the target relationship between circADAMTS6 and miR-431-5p. Results: After treatment with IL-1β, circADAMTS6 was down-regulated compared to the normal chondrocyte group. The overexpression of circADAMTS6 inhibited apoptosis in human chondrocytes, as indicated by annexin-V-FITC double staining. However, overexpression of miR-431-5p had the opposite effect. A dual luciferase reporter assay indicated that circADAMTS6 could directly binding with miR-431-5p. Conclusions: Our findings demonstrate that the circADAMTS6/miR-431-5p axis comprises a new target for OA. Bioinformatic analysis suggested that circADAMTS6 acted as a sponge of miR-431-5p.

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“…Numerous studies have been revealed that miRNAs serve as suppressors in the levels of inflammatory factors of multiple diseases [35][36][37][38], including in DN in vitro [20][21][22]. ICAM-1 has been confirmed to distinctly up-regulate in DN in vitro [42][43][44][45].…”

Section: Snhg15 Knockdown Promotes the Viability And Inhibits Inflammatory Response Of Hg-induced Hgmcs By Regulating Mir-141/icam-1mentioning

confidence: 99%

SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axisin vitro

et al. 2021

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Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). The present study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.

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Long non-coding RNA SNHG15 is a competing endogenous RNA of miR-141-3p that prevents osteoarthritis progression by upregulating BCL2L13 expression

Cited by 31 publications

References 31 publications

Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 15 (SNHG15) Alleviates Osteoarthritis Progression by Regulation of Extracellular Matrix Homeostasis

Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 15 (SNHG15) Alleviates Osteoarthritis Progression by Regulation of Extracellular Matrix Homeostasis

CircADAMTS6/miR‐431‐5p axis regulate interleukin‐1β induced chondrocyte apoptosis

SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axisin vitro

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