LncRNA FOXD2-AS1 induces chondrocyte proliferation through sponging miR-27a-3p in osteoarthritis

Wang, Yang; Cao, Lei; Wang, Qiugen; Huang, Jianhua; Xu, Shuogui

doi:10.1080/21691401.2019.1596940

Cited by 52 publications

(32 citation statements)

References 25 publications

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“…Overexpression of CASC2 can inhibit chondrocyte proliferation and promote chondrocyte apoptosis by upregulation of IL-17 [ 36 ]. lncRNA FOXD2-AS1 overexpression promotes proliferation of chondrocytes via sponging miR-27a-3p in OA [ 37 ]. In this study, our findings showed that lncRNA SNHG15 was underexpressed in OA cartilage tissues and IL-1β-induced chondrocytes.…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…H19 sensitivity to cytokine stimulation and serum starvation is thought to be important for synovial tissue dedifferentiation, ongoing inflammation and oxidative stress. Several studies in the last 2 years report inflammation‐associated lncRNAs in osteoarthritis including PVT1, 102 DANCR, 103 XIST, 104 H19, 105 FOXD2‐AS1 106 and MFI2‐AS1 107 . Although these studies do not focus on adiposity, the implication of lncRNAs in OA is clear, and given that the majority of OA patients have significantly increased levels of adiposity, further investigations may help stratify patients for specific diagnostics and therapies.…”

Section: Lncrnas and Obesity‐associated Chronic Inflammatory Diseasementioning

confidence: 99%

Involvements of long noncoding RNAs in obesity‐associated inflammatory diseases

et al. 2020

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Summary Obesity is associated with chronic low‐grade inflammation that affects the phenotype of multiple tissues and therefore is implicated in the development and progression of several age‐related chronic inflammatory disorders. Importantly, a new family of noncoding RNAs, termed long noncoding RNAs (lncRNAs), have been identified as key regulators of inflammatory signalling pathways that can mediate both pretranscriptional and posttranscriptional gene regulation. Furthermore, several lncRNAs have been identified, which are differentially expressed in multiple tissue types in individuals who are obese or in preclinical models of obesity. In this review, we examine the evidence for the role of several of the most well‐studied lncRNAs in the regulation of inflammatory pathways associated with obesity. We highlight the evidence for their differential expression in the obese state and in age‐related conditions including insulin resistance, type 2 diabetes (T2D), sarcopenia, osteoarthritis and rheumatoid arthritis, where obesity plays a significant role. Determining the expression and functional role of lncRNAs in mediating obesity‐associated chronic inflammation will advance our understanding of the epigenetic regulatory pathways that underlie age‐related inflammatory diseases and may also ultimately identify new targets for therapeutic intervention.

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“…It is closely related to pathological processes such as tumorigenesis, virus replication, inflammatory injury and so on. [3][4][5][6] In recent years, lncRNA has also been linked to the development of sepsis. 7,8 Cytoskeleton regulator RNA (CYTOR) is situated on human chromosome 2p11.2, and its abnormal expression is related to the inflammatory response and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

“…Long non‐coding RNA (lncRNA) is a kind of non‐coding RNA, whose transcriptional length is more than 200 nt. It is closely related to pathological processes such as tumorigenesis, virus replication, inflammatory injury and so on . In recent years, lncRNA has also been linked to the development of sepsis .…”

Section: Introductionmentioning

confidence: 99%

LncRNA CYTOR attenuates sepsis‐induced myocardial injury via regulating miR‐24/XIAP

Chen

Zhu

2020

Cell Biochemistry & Function

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This work aims to investigate the function and mechanism of long non-coding RNA (lncRNA) cytoskeleton regulator RNA (CYTOR) in myocardial injury induced by sepsis. The sepsis-induced myocardial injury model in mice was established by intraperitoneal injection of LPS (10 mg/kg) in vivo, and cardiomyocyte H9c2 was treated with LPS to mimic sepsis in vitro. CYTOR expression and miR-24 expression were detected by qRT-PCR. After up-regulation or down-regulation of CYTOR and miR-24 expression in the H9c2 cells, and the viability of the cells was detected via MTT assay, and cell apoptosis was detected by TUNEL assay. Western blot was applied to determine the expression level of caspase 3, Bax and X-chromosome-linked inhibitor of apoptosis (XIAP). Interaction between CYTOR and miR-24 was determined by bioinformatics analysis, RT-PCR and dual luciferase reporter assay. Interaction between miR-24 and XIAP was determined through bioinformatics analysis, RT-PCR, western blot and dual luciferase reporter assay. CYTOR was markedly down-regulated. CYTOR interacted with miR-24, and negatively regulated its expression level. Over-expression of CYTOR or transfection of miR-24 inhibitors significantly promoted viability and inhibited apoptosis of H9c2 cells, while the knockdown of CYTOR and transfection of miR-24 mimics had opposite effects. CYTOR suppressed the expression level of apoptosis-related proteins, but miR-24 increased them. miR-24 directly targeted the 3'UTR of XIAP, and suppressed it, and XIAP was modulated indirectly by CYTOR. Down-regulation of CYTOR aggravates sepsis-induced cardiac injury via regulating miR-24 and XIAP.

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LncRNA FOXD2-AS1 induces chondrocyte proliferation through sponging miR-27a-3p in osteoarthritis

Cited by 52 publications

References 25 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

Involvements of long noncoding RNAs in obesity‐associated inflammatory diseases

LncRNA CYTOR attenuates sepsis‐induced myocardial injury via regulating miR‐24/XIAP

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