Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis

Sun, Taitao; Yu, Jian; Han, Liang; Tian, Shuo; Xu, Bin; Gong, Xianbin; Zhao, Qiang; Wang, Yan

doi:10.1159/000487175

Cited by 27 publications

(17 citation statements)

References 34 publications

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“…Li, et al21 reported that LPS triggers cell proliferation, suppresses apoptosis, and enhances the release of IL-1β, IL-6, IL-12, and TNF-α in gastric cancer. Our study showed that LPS significantly induces chondrocyte injury, reflected by decreased cell viability, increased apoptosis, and stimulation of IL-1β, IL-6, and TNF-α secretion in C28/I2 cells, which was similar with previous research reported by Sun, et al22…”

Section: Discussionsupporting

confidence: 92%

Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis

Zou

2019

Yonsei Med J

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PurposeOsteoarthritis (OA) is a commonly occurring illness without a definitive cure, at present. Long non-coding RNAs (lncRNAs) have been widely confirmed to be involved in the modulation of OA progression. This study aimed to investigate the role and mechanism of lncRNA H19 in OA.Materials and MethodsAbundances of H19 and microRNA-130a (miR-130a) in lipopolysaccharide (LPS)-treated C28/I2 cells were measured by reverse-transcription quantitative PCR (RT-qPCR). CCK-8 and flow cytometry analyses were carried out to assess cell viability and apoptosis. Starbase online software was used to predict the putative binding sites between H19 and miR-130a. Luciferase reporter, RNA pull down, and RT-qPCR were performed to analyze the true interaction between H19 and miR-130a.ResultsA notably dose-dependent elevation of H19 levels was observed in LPS-treated C28/I2 cells. Knockdown of H19 ameliorated the injury of LPS-induced C28/I2 cells, reflected by induced viability, decreased apoptosis, and reduced inflammatory factor secretions. Moreover, H19 negatively regulated the expression of miR-130a via acting as a molecular sponge for miR-130a. The stimulatory effects of H19 on cell damage were abolished following the restoration of miR-130a.ConclusionLncRNA H19 aggravated the injury of LPS-induced C28/I2 cells by sponging miR-130a, hinting a novel regulatory mechanism and a potential therapeutic target for OA.

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Section: Discussionsupporting

confidence: 92%

Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis

Zou

2019

Yonsei Med J

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“…LncRNA MEG3 promoted chondrocytes apoptosis and inhibited cell proliferation through miR-16/SMAD7 axis 31 . LncRNA RP11-445H22.4 acting as a ceRNA against miR-301a, aggravated IL-1β-induced injury in OA progression 32 . In regard to HOTAIR, lots of studies verified that HOTAIR exerted its function by antagonizing the miRNAs effects and regulating the expression of miRNAs endogenous targets in many diseases.…”

Section: Discussionmentioning

confidence: 97%

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

et al. 2018

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Osteoarthritis (OA) is a chronic joint disease and hard to cure at present. Accumulating evidence suggests long noncoding RNA-HOTAIR (lncRNA-HOTAIR) plays important role in OA progression. However, the underlying molecular mechanism of HOTAIR in OA progression has not been well elucidated. In the present study, we identified that HOTAIR level was upregulated in OA cartilage tissues. High expression of HOTAIR was correlated with modified Mankin scale, extracellular matrix (ECM) degradation and chondrocytes apoptosis. The expression of miR-17-5p was down-regulated, while alpha-1, 2 fucosyltransferase 2 (FUT2) was increased in OA progression. Luciferase reporter and RNA immunoprecipitation (RIP) assays indicated that HOTAIR could directly bind to miR-17-5p and indirectly upregulate FUT2 level. Functional investigation revealed HOTAIR and FUT2 aggravated ECM degradation and chondrocytes apoptosis, and this effect could be reversed by miR-17-5p. Altered FUT2 modulated the activity of wnt/β-catenin pathway and HOTAIR/miR-17-5p also mediated wnt/β-catenin pathway through FUT2. Collectively, our findings indicated that HOTAIR/miR-17-5p/FUT2 axis contributed to OA progression via wnt/β-catenin pathway, which might provide novel insights into the function of lncRNA-driven in OA.

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“…Chondrocyte inflammatory responses are known to occur in the development of OA [14,15]. Lipopolysaccharide (LPS) triggers the immune system, and it is a major factor in the occurrence of osteolytic bone loss [16].…”

Section: Introductionmentioning

confidence: 99%

“…Lipopolysaccharide (LPS) triggers the immune system, and it is a major factor in the occurrence of osteolytic bone loss [16]. And it is widely adopted to construct cell injury model in vitro OA studies [14,16]. Therefore, an in vitro LPS-induced OA-like chondrocyte injury model was constructed in this study.…”

Section: Introductionmentioning

confidence: 99%

Sema4D Aggravated LPS-Induced Injury via Activation of the MAPK Signaling Pathway in ATDC5 Chondrocytes

Lei

Zhuang

et al. 2020

BioMed Research International

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Osteoarthritis (OA) is the most common chronic degenerative joint disease, and it remains the main cause of chronic disability in elderly individuals. Sema4D (semaphorin 4D) is involved in the immune system and related to bone injury, osteoporosis, osteoblast differentiation, and rheumatoid arthritis. However, the role of Sema4D in OA remains unclear. Hence, the LPS-stimulated chondrocyte cell injury model was constructed in this study to investigate the role of Sema4D in OA development. The results showed that Sema4D was increased in LPS-treated ATDC5 cells, and the knockdown of Sema4D suppressed the decline of cell viability, the increase of cell apoptosis, and the increase of IL-6, IL-1β, and TNF-α secretion in ATDC5 cells induced by LPS. Meanwhile, Sema4D overexpression aggravated the cell injury triggered by LPS, and inhibiting Plexin B1 partly abolished the effect of Sema4D overexpression on LPS-induced chondrocyte injury. Furthermore, silencing of Sema4D blocked the activation of the MAPK pathway in LPS-stimulated ATDC5 cells. Enhanced Sema4D promoted the activation of the MAPK pathway in LPS-stimulated ATDC5 cells. What is more, inhibiting the MAPK signaling pathway abolished the promoting effect of Sema4D overexpression on LPS-induced chondrocyte injury. Therefore, our study suggested that the knockdown of Sema4D protects ATDC5 cells against LPS-induced injury through inactivation of the MAPK signaling pathway via interacting with Plexin B1.

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Knockdown of Long Non-Coding RNA RP11-445H22.4 Alleviates LPS-Induced Injuries by Regulation of MiR-301a in Osteoarthritis

Cited by 27 publications

References 34 publications

Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis

Knockdown of LncRNA H19 Relieves LPS-Induced Damage by Modulating miR-130a in Osteoarthritis

Long non-coding RNA HOTAIR promotes osteoarthritis progression via miR-17-5p/FUT2/β-catenin axis

Sema4D Aggravated LPS-Induced Injury via Activation of the MAPK Signaling Pathway in ATDC5 Chondrocytes

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