Long non-coding RNA PVT1, a molecular sponge for miR-149, contributes aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes

Zhao, Yangxue; Zhao, Juan; Guo, Xufeng; She, Jiang; Liu, Yongjun

doi:10.1042/bsr20180576

Cited by 58 publications

(37 citation statements)

References 29 publications

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“…In line with our findings, the anti-apoptotic protein Bcl2 was enhanced, whereas the pro-apoptotic gene Bax was suppressed by silencing of signal transducer and activator of transcription 3 through delivering small interfering RNA in RA-FLSs [28]. Interestingly, PVT1 could directly bind to miR-149 as an endogenous sponge RNA and miR-149 suppression reversed the protective roles of PVT1 knockdown in attenuating IL-1β-evoked inflammation in osteoarthritic chondrocytes [29]. In addition, silencing of PVT1 promoted cell proliferation, yet suppressed inflammation in C28/I2 cells stimulated by IL-1β, which was counteracted by the deficiency of its target miR-27b-3p [30].…”

Section: Discussionsupporting

confidence: 88%

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

Wang

Kong

et al. 2020

J Orthop Surg Res

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Background: Rheumatoid arthritis (RA), a kind of autoimmune disorder, is featured by many physical symptoms and proliferation of fibroblast-like synoviocytes (FLSs). The relevance of long non-coding RNAs (lncRNAs) in the progression of RA has been probed. Hence, the goal of this report was to investigate the action of plasmacytoma variant translocation 1 (PVT1), a lncRNA, in FLSs and the basic mechanism. Methods: Initially, RA rats were developed to evaluate the expression of PVT1, microRNA-543 (miR-543), and signal peptide-CUB-EGF-like containing protein 2 (SCUBE2) in synovial tissues. Enhancement or loss of PVT1 or miR-543 was achieved to explore their effects on proliferation, cell cycle, and apoptosis of FLSs. The interaction between PVT1 and miR-543 and between miR-543 and its putative target SCUBE2 was examined to elucidate the correlations. Finally, the protein expression of proliferation-and apoptosis-associated genes were assessed by western blot assays. Results: PVT1 was overexpressed in synovial tissues from RA patients through microarray expression profiles. The PVT1 and SCUBE2 expression was boosted, and miR-543 was reduced in synovial tissues of rats with RA. PVT1 specifically bound to miR-543, and miR-543 negatively regulated SCUBE2 expression. Overexpression of PVT1 or silencing of miR-543 enhanced SCUBE2 expression, thereby promoting proliferation and interleukin-1β (IL-1β) secretion, while inhibiting apoptosis rate of FLSs. Conversely, si-SCUBE2 reversed the role of miR-543 inhibitor. Conclusion:The key findings support that PVT1 knockdown has the potency to hinder RA progression by inhibiting SCUBE2 expression to sponge miR-543.

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Section: Discussionsupporting

confidence: 88%

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

Wang

Kong

et al. 2020

J Orthop Surg Res

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“…li et al (13) revealed that PVT1 enhancement facilitates cell apoptosis in chondrocytes in osteoarthritis. a previous study stated that increased PVT1 expression expedites inflammation and aberrant metabolic dysfunction in il-β-induced chondrocytes (38). PVT1 is associated with the development of hyperglycemia-induced collagen degradation in chondrocytes (36).…”

Section: Discussionmentioning

confidence: 91%

“…Previous studies suggest that PVT1 can be used as a sponge for mirnas to participate in the development of osteoarthritis (13,38,39). mir-93-5p-containing exosomes attenuated the myocardial injury caused by acute myocardial damage (40).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of exosome‑mediated lnc‑PVT1 alleviates lipopolysaccharide‑induced osteoarthritis progression by mediating the HMGB1/TLR4/NF‑κB pathway via miR‑93‑5p

et al. 2020

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osteoarthritis is a chronic degenerative joint disease. long non-coding rna plasmacytoma variant translocation 1 (PVT1) is involved in the progression of osteoarthritis and exosomes serve a central role in intercellular communication. However, whether PVT1 can be mediated by exosomes in osteoarthritis has not been reported. Whole blood was drawn from osteoarthritis patients and healthy volunteers. lipopolysaccharide (lPS) was used to stimulate human normal chondrocytes (c28/i2) to construct a cell damage model in vitro. Protein levels were examined via western blot analysis. eThe expression of PVT1, microrna (mir)-93-5p and high mobility groupprotein B1 (HMGB1) was evaluated through reverse transcription-quantitative Pcr. cell viability and apoptosis were determined through ccK-8 or flow cytometric assay. inflammatory cytokines were measured via eliSa. The relationship between PVT1 or HMGB1 and miR-93-5p was confirmed by dual-luciferase reporter assay. PVT1, HMGB1 and exosomal PVT1 were upregulated while mir-93-5p was downregulated in osteoarthritis patient serum and lPS-induced c28/i2 cells. exosomes from osteoarthritis patient serum and lPS-treated c28/i2 cells increased PVT1 expression in c28/i2 cells. PVT1 depletion reversed the decrease of viability and the increase of apoptosis, inflammation responses and collagen degradation of C28/I2 cells induced by lPS. PVT1 regulated HMGB1 expression via sponging mir-93-5p. mir-93-5p inhibition abolished PVT1 silencing-mediated viability, apoptosis, inflammation responses and collagen degradation of lPS-stimulated c28/i2 cells. HMGB1 increase overturned mir-93-5p upregulation-mediated viability, apoptosis, inflammation responses and collagen degradation of lPS-stimulated c28/i2 cells. Furthermore, PVT1 modulated the Toll-like receptor 4/nF-κB pathway through an mir-93-5p/HMGB1 axis. in summary, exosome-mediated PVT1 regulated lPS-induced osteoarthritis progression by modulating the HMGB1/Tlr4/nF-κB pathway via mir-93-5p, providing a new route for possible osteoarthritis treatment.

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“…Furthermore, this study also found that silencing LINC01534 significantly reduced the contents of PGE2, NO, IL-6, IL-8, and TNF-α in the chondrocyte supernatant induced by IL-1β, while miR-140-5p inhibitor showed the opposite effect. Zhao et al found that lncRNA PVT1 inhibited the expression of aggrecan and collagen II in IL-1β-induced OA chondrocytes by targeting miR-149, up-regulated the secretions of MMPs, TNF-α, IL-8, IL-6, NO, and PGE2, and ultimately aggravated chondrocyte catabolism and inflammation (36).…”

Section: Discussionmentioning

confidence: 99%

LINC01534 Promotes the Aberrant Metabolic Dysfunction and Inflammation in IL-1β-Simulated Osteoarthritic Chondrocytes by Targeting miR-140-5p

Wei

Wang

et al. 2019

CARTILAGE

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Objective Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction in OA chondrocytes induced by interleukin-1β (IL-1β). Methods The quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II, and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The expressions of aggrecan and collagen II in the chondrocyte were detected by Western blot. The levels of tumor necrosis factor–α (TNF-α), IL-8, IL-6, MMP-13, MMP-9, MMP-3, and prostaglandin E2 (PGE2) in chondrocyte were determined by enzyme-linked immunosorbernt assay. Bioinformatics, dual luciferin gene reporting, RNA pulldown, and Northern blot were used to determine the interaction between LINC01534 and miR-140-5p. Results The results showed that LINC01534 was upregulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly downregulated the expression of matrix metalloproteinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also significantly inhibited the productions of proinflammatory factors NO, PGE2, TNF-α, IL-6, and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was confirmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion Therefore, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.

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Long non-coding RNA PVT1, a molecular sponge for miR-149, contributes aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes

Cited by 58 publications

References 29 publications

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

Knockdown of exosome‑mediated lnc‑PVT1 alleviates lipopolysaccharide‑induced osteoarthritis progression by mediating the HMGB1/TLR4/NF‑κB pathway via miR‑93‑5p

LINC01534 Promotes the Aberrant Metabolic Dysfunction and Inflammation in IL-1β-Simulated Osteoarthritic Chondrocytes by Targeting miR-140-5p

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