LncRNA
            <i>PTPRE-AS1</i>
            modulates M2 macrophage activation and inflammatory diseases by epigenetic promotion of PTPRE

Han, Xiao; Huang, Saihua; Xue, Ping; Fu, Jinrong; Liu, Lijuan; Zhang, Caiyan; Yang, Lan; Li, Xia; Sun, Licheng; Huang, Shau Ku; Zhou, Yufeng

doi:10.1126/sciadv.aax9230

Cited by 84 publications

(81 citation statements)

References 40 publications

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“…The proposed mechanism is that PTPRE-AS1 associates with the chromatin modifying protein WDR5 and guides the deposition of H3K4me3 at the PTPRE promoter. In accordance with this model, reduced levels of PTPRE-AS1 and PTPRE is observed in PBMCs from patients with allergic asthma [79]. Additional lncRNAs, including NIFK-AS1, have been demonstrated to influence M2 polarization of macrophages downstream of IL-4 signaling [80].…”

Section: Lncrna Modes Of Action: Nuclear Activitysupporting

confidence: 64%

“…A transcriptome-wide analysis of lncRNAs in bone marrow-derived macrophages (BMDMs) identified the lncRNA PTPRE-AS1 as being significantly induced during the IL-4 mediated maturation of M2 macrophage. [79]. PTPRE-AS1 s genomic position maps to opposite strand of the gene encoding tyrosine phosphatase receptor type E (PTPRE).…”

Section: Lncrna Modes Of Action: Nuclear Activitymentioning

confidence: 99%

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ncRNAs in Type-2 Immunity

Guidi¹,

Wedeles²,

Wilson³

2020

ncRNA

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Immunological diseases, including asthma, autoimmunity and immunodeficiencies, affect a growing percentage of the population with significant unmet medical needs. As we slowly untangle and better appreciate these complex genetic and environment-influenced diseases, new therapeutically targetable pathways are emerging. Non-coding RNA species, which regulate epigenetic, transcriptional and translational responses are critical regulators of immune cell development, differentiation and effector function, and may represent one such new class of therapeutic targets. In this review we focus on type-2 immune responses, orchestrated by TH2 cell-derived cytokines, IL-4, IL-5 and IL-13, which stimulate a variety of immune and tissue responses- commonly referred to as type-2 immunity. Evolved to protect us from parasitic helminths, type-2 immune responses are observed in individuals with allergic diseases, including Asthma, atopic dermatitis and food allergy. A growing number of studies have identified the involvement of various RNA species, including microRNAs (miRNA) and long non-coding (lncRNA), in type-2 immune responses and in both clinical and pre-clinical disease settings. We highlight these recent findings, identify gaps in our understanding and provide a perspective on how our current understanding can be harnessed for novel treat opportunities to treat type-2 immune-mediated diseases.

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Section: Lncrna Modes Of Action: Nuclear Activitysupporting

confidence: 64%

Section: Lncrna Modes Of Action: Nuclear Activitymentioning

confidence: 99%

ncRNAs in Type-2 Immunity

Guidi¹,

Wedeles²,

Wilson³

2020

ncRNA

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“…Researchers have suggested that in ammatory cytokines, especially NF-κΒ play a critical role in regulating lncRNAs in human diseases [9]. miR-489 targeting CHRF in repressing MyD88 and Smad in pulmonary brosis [10], differential expressed NEAT1 correlated with increased in ammation was observed in COPD [11], protein phosphatase ε (PTPRE) was involved in accelerating pulmonary allergic in ammation [12]. Therefore, we hypothesized that speci c lncRNAs might regulate the pathologic processes underlying pulmonary in ammation.…”

Section: Introductionmentioning

confidence: 97%

Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade

Chen

Zhang

Xiao

et al. 2020

Preprint

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Objective: To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under treatment of Dexamethasone (Dex).Methods: IL-1β (10 ng/mL) and LPS (1 μg/mL) was used to induce an inflammatory cell model with A549 cells, and the results showed that IL-1β performed better against LPS. Dex with different concentration was used to attenuate inflammation by IL-1β, and its effect was assessed by RT-PCR to detect the inflammatory related mRNA, including IKβ-α, IKKβ, IL-6, IL-8, and TNF-α. And ELISA to detect the inflammatory cytokines TNF-α, IL-6 and IL-8. RT-PCR was used to quantify levels of lncRNAs, including lncMALAT1, lncHotair, lncH19, and lncNeat1. LncH19 was most closely correlated with the inflammatory response, which was induced by IL-1β and attenuated by Dex. Among the lncRNAs, the level of lncH19 exhibited the highest increase following treatment with 1 μM and 10 μM Dex. Therefore, lncH19 was selected for further function study. LncH19 expression was inhibited by shRNA transduced by lentivirus. Cell assays for cell proliferation and apoptosis as well as RT-PCR, western blot, and ELISA for inflammatory related genes were conducted to confirm the functions of lncH19. Predicted target miRNAs of lncH19 included the following: hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p and hsa-miR-19a-3p. Following estimation by RT-PCR, hsa-miR-346, hsa-miR-18a-3p and hsa-miR-324-3p showed consistent patterns in A549 NC and A549 shlncH19. miRNA inhibitor was transfected into A549 NC and A549 shlncH19cells, and expression levels were determined by RT-PCR. Hsa-miR-324-3p was inhibited the most relative to hsa-miR-346 and hsa-miR-18a-3p and was subjected to further function study. RT-PCR, ELISA and western blotting for inflammatory related genes detection were conducted to validate the functions of the target hsa-miR-324-3p.Results: Dex with 1 μM and 10 μM were shown to be effective in attenuating the inflammatory response. During this process, lncH19 significantly increased in expression (P < 0.05). Dex with 1 μM was for further study. Under IL-1β treatment with or without Dex, the inhibition of lncH19 lead to an increase cell proliferation, a decrease in cell apoptosis, an increase in the protein level of inflammatory-related genes, the phosphorylation of P65, ICAM-1 and VCAM-1, and inflammatory cytokines. Following prediction of the targets of lncH19 and validation by RT-PCR, miR-346, miR-18a-3p and miR-324-3p were found to be negatively correlated to lncH19. Additionally, Dex increased the expression of lncH19, but the expression of the miRNAs was reduced. Among miRNAs, miR-324-3p was the most markedly down-regulated following treatment of miRNA inhibitors. The MTS assay and cell apoptosis assay showed that the miR-324-3p inhibitor inhibited cell proliferation and induced cell apoptosis, thereby significantly attenuating the inflammatory response, which reversed the effect of lncH19 in regulating cell proliferation and the secretion of inflammatory cytokines (P < 0.05). Therefore, lncH19 might regulate miR-324-3p during Dex treatment in pulmonary inflammatory response.Conclusion: Dex can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade.

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“…Next, we investigated the role of lnc-BAZ2B and its cis target gene BAZ2B in a mouse model of M2 macrophage-associated, CRE-induced pulmonary inflammation (Fig 5, A). 38 Asthma pathologies developed in CRE-challenged mice, as indicated by the significant recruitment of inflammatory cells to the lung, with dense peribronchial infiltrates and goblet cell hyperplasia in the histologic examination; however, this was not observed in PBS-challenged mice (Fig 5, B). Interestingly, lnc-BAZ2B overexpression in CRE-treated mice significantly enhanced pulmonary inflammation, including increased peribronchial infiltrates and goblet cell hyperplasia, and it increased the total number of infiltrated inflammatory cells, especially eosinophils, in bronchoalveolar lavage fluid and enhanced the expression level of Muc5ac, compared with that in mice treated with CRE only (Fig 5, B-E).…”

Section: Lnc-baz2b and Baz2b Exacerbate Cre-induced Lung Inflammationmentioning

confidence: 91%

lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma through stabilizing BAZ2B pre-mRNA

Wang

Liu

et al. 2021

Journal of Allergy and Clinical Immunology

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LncRNA PTPRE-AS1 modulates M2 macrophage activation and inflammatory diseases by epigenetic promotion of PTPRE

Abstract: PTPRE-AS1 deficiency aggravates pulmonary inflammation but reduces colitis severity by modulating M2 macrophage activation.

Cited by 84 publications

References 40 publications

ncRNAs in Type-2 Immunity

ncRNAs in Type-2 Immunity

Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade

lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma through stabilizing BAZ2B pre-mRNA

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