NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

Xu, Jing; Jiang, Congshan; Zhu, Wenhua; Wang, B.; Jin, Yan; Min, Zixin; Geng, Manman; Han, Yong; Ning, Qilan; Zhang, F.; Sun, Jian; Meng, Liesu; Lu, Shemin

doi:10.1016/j.joca.2015.04.016

Cited by 18 publications

(15 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3e ). In addition, ITS treatment was applied to cultured cells for 14 days as described previously to induce ATDC5 cells to differentiate in vitro [ 29 ], and then the expression of mmu-miR-181a-5p , Sbp2 and SBP2 was detected. With chondrocyte differentiation, the expression of mmu-miR-181a-5p showed remarkable up-regulation at D3 ( P = 0.0258), D7 ( P = 0.0178) and D14 ( P = 0.0103), while SBP2 protein expression was significantly reduced, although the expression of Sbp2 was almost constant (Fig.…”

Section: Resultsmentioning

confidence: 99%

The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis

Xue

Min

Xia

et al. 2018

BMC Musculoskelet Disord

View full text Add to dashboard Cite

BackgroundThe phenotypes of osteoarthritis (OA) consist of cartilage extracellular matrix (ECM) metabolism disorder and the breakdown of cartilage homeostasis, which are induced by pro-inflammatory factors and oxidative stress. Selenoproteins regulated by selenocysteine insertion sequence binding protein 2 (SBP2) are highly effective antioxidants, but their regulatory mechanisms, particularly the involvement of miRNAs, are not fully understood.MethodsTo explore whether miR-181a-5p and SBP2 are involved in OA pathogenesis, we established an IL-1β model using the chondrocyte SW1353 cell line. Next, we up- or down-regulated SBP2 and miRNA-181a-5p expression in the cells. Finally, we measured the expression of miRNA-181a-5p, SBP2 and three selenoproteins in OA cartilage and peripheral blood.ResultsThe results showed that IL-1β increased hsa-miR-181a-5p and decreased SBP2 in a time- and dose-dependent manner. GPX1 and GPX4, which encode crucial glutathione peroxidase antioxidant enzymes, were up-regulated along with SBP2 and miR-181a-5p. Furthermore, SBP2 showed a significant negative correlation with miR-181a-5p during induced ATDC5 cell differentiation. There was lower GPX1 and GPX4 mRNA expression and SBP2 protein expression in damaged cartilage than in smooth cartilage from the same OA sample, and hsa-miR-181a-5p expression on the contrary. Similar results were observed in peripheral blood. In conclusion, we have reported a novel pathway in which pro-inflammatory factors, miRNA, SBP2 and selenoproteins are associated with oxidation resistance in cartilage.ConclusionOverall, this study provides the first comprehensive evidence that pro-inflammatory factors cause changes in the cartilage antioxidant network and describes the discovery of novel mediators of cartilage oxidative stress and OA pathophysiology. Our data suggest that miR-181a-5p may be used to develop novel early-stage diagnostic and therapeutic strategies for OA.Electronic supplementary materialThe online version of this article (10.1186/s12891-018-2273-6) contains supplementary material, which is available to authorized users.

show abstract

Section: Resultsmentioning

confidence: 99%

The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis

Xue

Min

Xia

et al. 2018

BMC Musculoskelet Disord

View full text Add to dashboard Cite

show abstract

“…T-2 toxin signicantly increases the levels of ROS and depletes intracellular reduced glutathione GSH. [13][14][15] That leads to single-strand breaks in DNA and the cells apoptosis is triggered. T-2 toxin causes a large range of toxic effects in animals, such as weight loss, decreases in blood cell and leukocyte count, reduction in plasma glucose, and pathological changes in the liver and stomach.…”

Section: Discussionmentioning

confidence: 99%

Identification and characterization of a T-2 toxin-producingFusarium poaestrain and the anti-tumor effect of the T-2 toxin on human hepatoma cell line SMMC-7721

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Moreover, ATDC5 cells were dealt with series concentrations (0.1, 1, 5, 10, 15, 20 mM) of MF (Sigma) and precultured in an incubator at 37°C for 2 h before LPS inducement. Additionally, ATDC5 cells were pretreated with 10 mM of NAC [N-acetylcysteine, a scavenger of reactive oxygen species (ROS)] (Sigma) at 37°C for 1 h before LPS inducement to serve as the positive control of MF treatment (Xu et al, 2015a).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

“…Additionally, for investigation of the signal pathways, the LPS + MF treated ATDC5 cells were respectively incubated with the PI3K inhibitor Wortmannin (MedChemExpress, New Jersey, USA) (10 m M , 1 h ) , P T E N i n h i b i t o r V O -O H p i c t r i h y d r a t e (MedChemExpress) (10 nM, 1 h), AKT inhibitor MK2206 (MedChemExpress) (200 nM, 30 min) and NF-kB pathway inhibitor pyrrolidine dithiocarbamate (PDTC) (Sigma) (10 mM, 30 min) reference to earlier published literatures (Xu et al, 2015a;Lu et al, 2017;Guo et al, 2018;Masarwi et al, 2018).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Liu

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Background: Mangiferin (MF) was reported to possess anti-inflammatory activity. This investigation tried to probe into the underlying mechanism of MF in osteoarthritis.Methods: ATDC5 cells were pretreated with series concentrations of MF (0.1, 1, 5, 10, 15, 20 mM) for 2 h and then were exposed to lipopolysaccharide (LPS) (5 mg/ml) for 12 h to construct the inflammatory injury model. The cell viability, productions of pro-inflammatory cytokines and enzymes were respectively measured by employing CCK-8 assay, western blot, ELISA, and quantitative reverse-transcription (qRT)-PCR. miR-181a expression was altered by employing cell transfection. Dichloro-dihydro-fluorescein diacetate (DCFH-DA) method was employed for detection of reactive oxygen species (ROS) generation. Dual luciferase activity assay was conducted for analyzing the relationship between miR-181a and PTEN. The underlying mechanism was determined by employing western blot.Results: High doses of MF treatment (15 and 20 mM) noticeably induced inflammatory injury exhibiting as increased the productions of pro-inflammatory cytokines, enzymes and ROS, activated NF-kB pathway and deactivated PTEN/PI3K/AKT pathway in ATDC5 cells. Besides, MF treatment notably remitted LPS-induced inflammatory injury through deactivation of NF-kB pathway and activation of PTEN/PI3K/AKT pathway. PTEN was a target of miR-181a. Inhibition of miR-181a remarkably reversed MF-triggered impacts on ATDC5 cells.Conclusion: MF attenuated LPS-induced inflammatory damage through miR-181a/ PTEN axis and thereby inhibiting NF-kB pathway and activating PI3K/AKT pathway.

show abstract

NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

Cited by 18 publications

References 37 publications

The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis

The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis

Identification and characterization of a T-2 toxin-producingFusarium poaestrain and the anti-tumor effect of the T-2 toxin on human hepatoma cell line SMMC-7721

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Contact Info

Product

Resources

About