Astrocyte elevated gene-1 promotes inflammation and invasion of fibroblast-like synoviocytes in rheumatoid arthritis

Hong, Ruilong; Wang, Kun; Shi, Hanyu

doi:10.1016/j.tice.2017.09.005

Cited by 9 publications

(7 citation statements)

References 36 publications

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“…A recent study demonstrated AEG‐1 interacted with p65 subunit of NF‐κB and contributed to the production of inflammatory cytokines in rheumatic arthritis (Hong et al . ). These studies indicated the importance of AEG‐1 in inflammatory and emphasized the interaction between AEG‐1 and NF‐κB signalling.…”

Section: Introductionmentioning

confidence: 97%

“…Besides the discovery in cancer research, elevated AEG-1 expression in astrocytes has been reported to enhance the inflammatory response of the nervous system in HIV infection by promoting NF-jB activation (Vartak-Sharma et al 2014). A recent study demonstrated AEG-1 interacted with p65 subunit of NF-jB and contributed to the production of inflammatory cytokines in rheumatic arthritis (Hong et al 2017). These studies indicated the importance of AEG-1 in inflammatory and emphasized the interaction between AEG-1 and NF-jB signalling.…”

Section: Introductionmentioning

confidence: 99%

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Astrocyte elevated gene‐1 participates in the production of pro‐inflammatory cytokines in dental pulp cells via NF‐κB signalling pathway

Yang

et al. 2018

Int Endodontic J

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Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Astrocyte elevated gene‐1 participates in the production of pro‐inflammatory cytokines in dental pulp cells via NF‐κB signalling pathway

Yang

et al. 2018

Int Endodontic J

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“…Its overexpression promotes tumor proliferation, diffusion, metastasis, neovascularization, and chemotherapeutic drug resistance in malignant tumors (Emdad et al, 2007;Meng et al, 2013). Recently, the role of AEG-1 in promoting the inflammatory cytokines release, migration, and invasion of rheumatoid fibroblast-like synoviocytes was determined (Hong et al, 2017). Recently, the role of AEG-1 in promoting the inflammatory cytokines release, migration, and invasion of rheumatoid fibroblast-like synoviocytes was determined (Hong et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Most noncancerous roles of the AEG-1 were identified in studies of the neurological disorders of CNS (Noch and Khalili, 2013;Yin and Feng, 2017). Recently, the role of AEG-1 in promoting the inflammatory cytokines release, migration, and invasion of rheumatoid fibroblast-like synoviocytes was determined (Hong et al, 2017). Moreover, researchers suggested that AEG-1 interacted with NF-kB signaling in dental pulp and it played an important role in inflammatory (Wu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Silencing astrocyte elevated gene‐1 attenuates lipopolysaccharide‐induced inflammation and mucosal barrier injury in NCM460 cells by suppressing the activation of NLRP3 inflammasome

Yang

Chen

2018

Cell Biology International

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The effect of oncogene astrocyte-elevated gene-1 (AEG-1) on noncancerous colonic epithelial cell disease is rarely studied. We aim to investigate the role of AEG-1 in lipopolysaccharide (LPS)-induced inflammation and mucosal barrier injury, and their potential mechanisms. NCM460 cells were stimulated by different concentrations of LPS at 12 h or 24 h. Cell viability and the expression of AEG-1 was determined by CCK-8, qRT-PCR, and Western blotting. Silencing AEG-1 was successfully established. Reactive oxygen species (ROS) level and apoptosis were measured by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was performed to detect IL-1b and IL-18 levels. qRT-PCR and Western blot were performed to assess the mRNA and protein level of tight junction (TJ)-associated genes, NLRP3 inflammasome activation-related factors. Silencing AEG-1 decreased ROS production; cell apoptosis; and IL-1b, IL-18 release, compared to those treated by LPS. Up-regulation of ZO-1 and Occludin showed that siAEG-1 could protect mucosal barrier from LPS-injured. Silencing AEG-1 could significantly inhibit NLRP3 and cleaved caspase-1 expression in LPS stimulation environment. Silencing AEG-1 inhibited NLRP3 activation, while the activation of caspase-1 reduced the secretion of proinflammatory cytokines IL-1b and IL-18. However, overexpressing AEG-1 aggravated LPS-triggered injury and activation of NLRP3 inflammasome.

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“…In addition, the TLR4 interactor with leucine-rich repeats (TRIL), a ligand of TLR4, is highly expressed in the spinal cord after IR [14]. Likewise, metadherin (MTDH) or astrocyte elevated gene 1 is upregulated in various tumors [15] and neurodegeneration diseases [16], and triggers the NF-κB pathway [17], although its potential role in spinal cord IR is unknown. Long non-coding RNAs (lncRNAs) are a class of non-coding transcripts longer than 200 bases [18] that regulate gene expression by targeting the miRNAs as endogenous RNAs (ceRNAs) [19].…”

mentioning

confidence: 99%

Downregulation of Long Noncoding RNA TUG1 Attenuate MTDH /NF-κB/IL-1β mediated inflammatory damage via Targeting miR-29b-1-5p After Spinal cord ischemia reperfusion in rats

Jia

Fang

et al. 2020

Preprint

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Background: Spinal cord ischemia reperfusion (IR) is associated with an inflammatory response. The long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) and microRNA-29b (miR-29b) family are frequently dysregulated in neuro-ischemic diseases. However, their potential roles in spinal cord IR injury (IR) are unknown. Methods: A spinal cord IR model was established in rats by14-minute occlusion of aortic arch. The aberrant miRNAs were identified by microarray analysis, and qRT-PCR was used to validate the lncRNA and microRNA levels. The motor function of the differentially-treated animals was assessed by Tarlov scores, and the leakage of Blood-spinal cord barrier (BSCB) was measured in terms of the extravasation of Evans blue (EB) dye. The expression levels of different proteins were analyzed by Western blotting and immunofluorescence. The interaction between TUG1 and miR-29b-1-5p, TRIL and miR-29b-1-5p, and MTDH and miR-29b-1-5p were determined using bioinformatics programs and the dual-luciferase reporter assay. Results: MiR-29b-1-5p was significantly downregulated and TUG1 was upregulated in the spinal cord of rats after IR. In addition, TRIL and MTDH protein levels were also significantly increased after IR. MTDH was predicted as a target of miR-29b-1-5p and its knockdown downregulated NF-κB and IL-1β levels. In addition, a direct interaction was observed between TUG1 and miR-29b-1-5p, and knocking down TUG1 upregulated the miRNA. Furthermore, overexpression of miR-29b-1-5p or TUG1 knockdown alleviated BSCB leakage and improved hind-limb motor function, and downregulated MTDH and its downstream pro-inflammatory cytokines. Suppression of miR-29b-1-5p reversed the neuroprotective effect of TUG1 knockdown, restored the levels of MTDH/ NF-κB/IL-1β and activated astrocytes. Conclusion: Downregulation of TUG1 alleviated MTDH/NF-κB/IL-1β pathway-mediated inflammatory damage after IR by targeting miR-29b-1-5p. Keywords: Spinal cord ischemia reperfusion injury, Neuroinflammation, Blood-spinal cord barrier, Astrocytes, TUG1, miR-29b-1-5p, MTDH

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Astrocyte elevated gene-1 promotes inflammation and invasion of fibroblast-like synoviocytes in rheumatoid arthritis

Cited by 9 publications

References 36 publications

Astrocyte elevated gene‐1 participates in the production of pro‐inflammatory cytokines in dental pulp cells via NF‐κB signalling pathway

Astrocyte elevated gene‐1 participates in the production of pro‐inflammatory cytokines in dental pulp cells via NF‐κB signalling pathway

Silencing astrocyte elevated gene‐1 attenuates lipopolysaccharide‐induced inflammation and mucosal barrier injury in NCM460 cells by suppressing the activation of NLRP3 inflammasome

Downregulation of Long Noncoding RNA TUG1 Attenuate MTDH /NF-κB/IL-1β mediated inflammatory damage via Targeting miR-29b-1-5p After Spinal cord ischemia reperfusion in rats

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