MiR-374b-5p Regulates T Cell Differentiation and Is Associated with rEg.P29 Immunity

Li, Dongjie; Du, Xiancai; Zhu, Mingzhao; Yang, Songhao; Zhao, Wei

doi:10.1155/2020/8024763

Cited by 6 publications

(5 citation statements)

References 42 publications

(72 reference statements)

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“…miR‐374b‐5p has been widely investigated in various cancers, cardiovascular diseases, and immune‐related diseases. 35 , 36 , 37 , 38 , 39 , 40 Moreover, Akbaba et al 41 have elaborated that miR‐374b‐5p acts as an inflammation‐related gene, indicating that miR‐374b‐5p may participate in inflammation‐related diseases. Furthermore, miR‐374b‐5p was shown to be elevated in postmenopausal osteoporosis, and its upregulation could suppress osteoblast differentiation and bone formation.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequently, our study validated the targeted association between miR‐374b‐5p and lncRNA MAGI2‐AS3 via functional experiments. miR‐374b‐5p has been widely investigated in various cancers, cardiovascular diseases, and immune‐related diseases 35–40 . Moreover, Akbaba et al 41 have elaborated that miR‐374b‐5p acts as an inflammation‐related gene, indicating that miR‐374b‐5p may participate in inflammation‐related diseases.…”

Section: Discussionmentioning

confidence: 99%

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Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

2023

Immunity Inflam & Disease

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Background: Intervertebral disc degeneration (IDD) is a pathological process that occurs during the natural aging of intervertebral discs. Accumulating evidence suggests that noncoding RNAs (ncRNAs), including microRNAs and long ncRNAs (lncRNAs), participate in the pathogenesis and development of IDD. Herein, we examined the role of lncRNA MAGI2-AS3 in the pathogenic mechanism of IDD.Material and Methods: To develop an IDD in vitro model, we treated human nucleus pulposus (NP) cells with lipopolysaccharide (LPS). Aberrant levels of lncRNA MAGI2-AS3, miR-374b-5p, interleukin (IL)-10 and extracellular matrix (ECM)-related proteins in NP cells were examined using reverse transcriptionquantitative PCR and western blot analysis. LPS-induced NP cell injury and inflammatory response were confirmed using the MTT assay, flow cytometry, Caspase3 activity, and enzyme-linked immunosorbent assay. Dual-luciferase reporter assay and rescue experiments were performed to confirm targets between lncRNA MAGI2-AS3 and miR-374b-5p or miR-374b-5p and IL-10. Results: LPS-induced NP cells exhibited low levels of lncRNA MAGI2-AS3 and IL-10 expression, along with high miR-374b-5p expression. miR-374b-5p was a target of lncRNA MAGI2-AS3 and IL-10. LncRNA MAGI2-AS3 ameliorated injury, inflammatory response, and ECM degradation in LPS-treated NP cells by downregulating miR-374b-5p to upregulate IL-10 expression. Conclusions: LncRNA MAGI2-AS3 increased IL-10 expression levels by sponging miR-374b-5p, which, in turn, alleviated LPS-triggered decreased NP cell proliferation and increased apoptosis, inflammatory response, and ECM degradation. Therefore, lncRNA MAGI2-AS3 may be a potential therapeutic target for IDD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

2023

Immunity Inflam & Disease

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“…After 6 h, the transfected cells were removed into a 24-well plate. For Th1 and Th2 cells activation, as previous reported [38]. The cells were used to do later experiment after transfection 96 h. expression.…”

Section: Cd4 + T Cd8 + T and B Cells Sortingmentioning

confidence: 99%

lncRNA028466 Regulates Th1/Th2 Cytokines Expression and Associated with Echinococcus Granulosus Antigen P29 Immunity

Wang

Yang

Niu

et al. 2021

Preprint

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Background: Cystic echinococcosis (CE) is a parasite disease that was caused by Echinococcus granulosus (Eg). The recombinant Echinococcus granulosus antigen P29 (rEg.P29) has been shown to conferred effective immunity to sheep and mice during Echinococcus granulosus secondary infection in our previous study. In our study, we strove to research the ability of Long noncoding RNA 028466 (lncRNA028466) as a regulator for the protective immunity mediated by rEg.P29 vaccination and studied the effects of lncRNA028466 on CD4+T cells differentiation in mice spleen.Methods: Female BALB/c mice were divided into two groups and were vaccinated subcutaneously with rEg.P29 antigen and PBS as a control (12 mice each group). Following prime-boost vaccination, CD4+T, CD8+T，and B cells from the spleen were isolated by flow cytometry. Quantitative real-time PCR (qRT-PCR) was performed to measure the expression of lncRNA028466 in these three kinds of cells. Then, lncRNA028466 was over-expressed and knock-downed. Furthermore, were d by qRT-PCR and ELISA were performed to evaluate the production of IFN-γ, IL-2, IL-4, and IL-10, as well as was flow cytometry was performed to detect the differentiation of Th1 and Th2 subgroups. Results: lncRNA028466 was significantly decreased after the second-week of immunization with rEg.P29 antigen. The proportion of CD4+T cells was increased after rEg.P29 immunization. Subsequent overexpression and knockdown of lncRNA028466 in naive CD4+T cells were performed to detect changes in Th1 and Th2 cytokines expression. Overexpression of lncRNA028466 facilitated the production of IL-4, IL-10 and suppressed the production of IFN-γ, IL-2. Furthermore, after transfection with siRNA028466, IL-2 production was facilitated and IL-10 production was suppressed in naive CD4+T cells.Conclusions: Immunization with rEg.P29 down-regulated the expression of lncRNA028466, which was related to a higher Th1 immune response, a higher Th2 immune response with lncRNA028466 overexpression, a higher IL-2 mRNA expression, and a lower IL-10 mRNA expression with lncRNA028466 knockdown. Our results suggest that lncRNA028466 may be involved in rEg.P29-mediated immune response by regulating cytokines expression of Th1 and Th2.

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“…Based on bioinformatics analysis and preceding reports, miR-374b-5p (gene ID: 100126317) is nominated as a potential target for MAGI2-AS3 as well as an upstream modulator of the PTEN/AKT/IRF-3/IFN-β cascade. ,, MiR-374b-5p, which is one of the non-coding RNAs ranging from 20 to 25 nucleotides in length, has been significantly studied in different disorders such as neurodegenerative conditions, encephalopathy, and amyotrophic lateral sclerosis. , In addition, the diminished expression of miR-374b-5p has been documented in neurodegenerative disorders such as Alzheimer’s and stimulates the proliferation and differentiation of neural stem cells, which play a pivotal role in neurogenesis . Yet, the roles of MAGI2-AS3 and miR-374b-5p were not elucidated in MS.…”

Section: Introductionmentioning

confidence: 99%

MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

Kortam

Elfar

Shaker

et al. 2023

ACS Chem. Neurosci.

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Multiple sclerosis (MS) is a chronic disease and one of the leading causes of disability in young adults. The current study aims to investigate the pathogenesis of MS via studying the regulatory role of novel lncRNA MAGI2-AS3 in miR-374b-5p and their downstream targets PTEN/AKT/IRF-3/IFN-β and the relationship of this pathway with disease severity. Moreover, it aims to assess the role of MAGI2-AS3/miR-374b-5p as diagnostic and/or prognostic biomarkers for MS. Overall, 150 contributors were recruited: 100 patients with MS and 50 healthy volunteers. Gene expression of MAGI2-AS3, miR-374b-5p, PTEN, AKT, and IRF-3 were assessed using RT-qPCR, and IFN-β was measured by ELISA. Compared with the healthy control group, serum MAGI2-AS3 and PTEN were downregulated in MS patients, whereas miR-374b-5p, PI3K, AKT, IRF-3, and IFN-β were upregulated in MS patients. Furthermore, MAGI2-AS3 was downregulated, while miR-374b-5p was upregulated in MS patients with an expanded disability status scale (EDSS) ≥3.5, compared to patients with an EDSS <3.5. Receiver-operating-characteristic curve analysis revealed that MAGI2-AS3 and miR-374b-5p can be used in the diagnosis of MS. Remarkably, multivariate logistic analysis revealed that MAGI2-AS3, miR-374b-5p, PTEN, and AKT act as independent variables in MS. Moreover, MAGI2-AS3 was directly correlated with PTEN and inversely correlated with miR-374b-5p, AKT, and EDSS. Regarding miR-374b-5p, it was positively correlated with AKT and EDSS. In conclusion, the study showed for the first time that the crosstalk between MAGI2-AS3 and miR-374b-5p could affect the AKT/IRF3/IFN-β axis in MS. Interestingly, MAGI2-AS3 and miR-374b-5p could be genetic noninvasive biomarkers for MS.

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MiR-374b-5p Regulates T Cell Differentiation and Is Associated with rEg.P29 Immunity

Cited by 6 publications

References 42 publications

Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

lncRNA028466 Regulates Th1/Th2 Cytokines Expression and Associated with Echinococcus Granulosus Antigen P29 Immunity

MAGI2-AS3 and miR-374b-5p as Putative Regulators of Multiple Sclerosis via Modulating the PTEN/AKT/IRF-3/IFN-β Axis: New Clinical Insights

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