LncRNA-MEG3 functions as a competing endogenous RNA to regulate Treg/Th17 balance in patients with asthma by targeting microRNA-17/ RORγt

Qiu, Yuling; Wu, Yan; Lin, Minjie; Bian, Tao; Xiao, Yonglong; Qin, Chu

doi:10.1016/j.biopha.2018.12.080

Cited by 112 publications

(106 citation statements)

References 34 publications

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“…However, no functional or mechanistic reports have been published thus far, at least to the best of our knowledge. Some studies have suggested the potential role of lncRNAs as ceRNAs (51)(52)(53); however, the mechanism of the discovered lncRNAs was not well defined.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA EBLN3P promotes the recovery of the function of impaired spiral ganglion neurons by competitively binding to miR‑204‑5p and regulating TMPRSS3 expression

et al. 2020

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Sensorineural hearing loss (SNHL) is one of the major leading causes of hearing impairment, and is typically characterized by the degeneration of spiral ganglion neurons (SGNs). In previous studies by the authors, it was demonstrated that microRNA (miRNA or miR)-204-5p decreased the viability of SGNs by inhibiting the expression of transmembrane protease, serine 3 (TMPRSS3), which was closely associated with the development of SGNs. However, the upstream regulatory mechanism of miR-204-5p was not fully elucidated. The present study found that an important upstream regulatory factor of miR-204-5p, long non-coding RNA (lncRNA) EBLN3P, was expressed at low levels in impaired SGNs, whereas it was expressed at high levels in normal SGNs. Mechanistic analyses demonstrated that lncRNA EBLN3P functioned as a competing endogenous RNA (ceRNA) when regulating miR-204-5p in normal SGNs. In addition, lncRNA EBLN3P regulated TMPRSS3 expression via the regulation of miR-204-5p in normal SGNs. In vitro functional analysis revealed that lncRNA EBLN3P promoted the recovery of the viability of normal SGNs and inhibited the apoptosis of normal SGNs. Finally, the results revealed a recovery-promoting effect of lncRNA EBLN3P on the structure and function of impaired SGNs in models of deafness. On the whole, the findings of the present study demonstrate that lncRNA EBLN3P promotes the recovery of the function of impaired SGNs by competitively binding to miR-204-5p and regulating TMPRSS3 expression. This suggests that lncRNA EBLN3P may be a potential therapeutic target for diseases involving SNHL.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA EBLN3P promotes the recovery of the function of impaired spiral ganglion neurons by competitively binding to miR‑204‑5p and regulating TMPRSS3 expression

et al. 2020

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“…Other Müller cell lncRNAs that show significant changes in response to T. gondii infection-MEG3, MIR17HG and lnc-SGK1-are involved in regulation of the Th17 immune response [43][44][45][46]. This adaptive immune response, and production of IL-17 and IL-23 in particular, has been strongly implicated in the pathogenesis of ocular toxoplasmosis [47,48].…”

Section: Discussionmentioning

confidence: 99%

“…This adaptive immune response, and production of IL-17 and IL-23 in particular, has been strongly implicated in the pathogenesis of ocular toxoplasmosis [47,48]. MEG3 is defined as a tumor suppressor, but also regulates the balance of Treg cells and Th17 cells; downregulation of MEG3 increases forkhead box P3 (FOXP3) expression and inhibits retinoic acid receptor-related orphan receptor γt (RORγt) expression, to tip the balance in favor of Treg cells [45,46]. On the other hand, MIR17HG and lnc-SGK1 promote the Th17 response [43,44].…”

Section: Discussionmentioning

confidence: 99%

Expression of Long Non-Coding RNAs by Human Retinal Müller Glial Cells Infected with Clonal and Exotic Virulent Toxoplasma gondii

Rochet

Appukuttan

et al. 2019

ncRNA

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Retinal infection with Toxoplasma gondii—ocular toxoplasmosis—is a common cause of vision impairment worldwide. Pathology combines parasite-induced retinal cell death and reactive intraocular inflammation. Müller glial cells, which represent the supporting cell population of the retina, are relatively susceptible to infection with T. gondii. We investigated expression of long non-coding RNAs (lncRNAs) with immunologic regulatory activity in Müller cells infected with virulent T. gondii strains—GT1 (haplogroup 1, type I) and GPHT (haplogroup 6). We first confirmed expression of 33 lncRNA in primary cell isolates. MIO-M1 human retinal Müller cell monolayers were infected with T. gondii tachyzoites (multiplicity of infection = 5) and harvested at 4, 12, 24, and 36 h post-infection, with infection being tracked by the expression of parasite surface antigen 1 (SAG1). Significant fold-changes were observed for 31 lncRNAs at one or more time intervals. Similar changes between strains were measured for BANCR, CYTOR, FOXD3-AS1, GAS5, GSTT1-AS1, LINC-ROR, LUCAT1, MALAT1, MIR22HG, MIR143HG, PVT1, RMRP, SNHG15, and SOCS2-AS1. Changes differing between strains were measured for APTR, FIRRE, HOTAIR, HOXD-AS1, KCNQ1OT1, LINC00968, LINC01105, lnc-SGK1, MEG3, MHRT, MIAT, MIR17HG, MIR155HG, NEAT1, NeST, NRON, and PACER. Our findings suggest roles for lncRNAs in regulating retinal Müller cell immune responses to T. gondii, and encourage future studies on lncRNA as biomarkers and/or drug targets in ocular toxoplasmosis.

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“…Another group revealed that lncRNA GAS5/miR-10a/BDNF regulatory axis contributed to the ASMCs proliferation [7]. In terms of asthma immunity, lncRNA MEG3 can regulate RORγt and affect Treg/Th17 balance via inhibiting miR-17 [8].…”

Section: Introductionmentioning

confidence: 99%

Construction of asthma related competing endogenous RNA network revealed novel long non-coding RNAs and potential new drugs

Liao

Wang

et al. 2020

Respir Res

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Background: Asthma is a heterogeneous disease characterized by chronic airway inflammation. Long non-coding RNA can act as competing endogenous RNA to mRNA, and play significant role in many diseases. However, there is little known about the profiles of long non-coding RNA and the long non-coding RNA related competing endogenous RNA network in asthma. In current study, we aimed to explore the long non-coding RNA-microRNA-mRNA competing endogenous RNA network in asthma and their potential implications for therapy and prognosis. Methods: Asthma-related gene expression profiles were downloaded from the Gene Expression Omnibus database, re-annotated with these genes and identified for asthma-associated differentially expressed mRNAs and long noncoding RNAs. The long non-coding RNA-miRNA interaction data and mRNA-miRNA interaction data were downloaded using the starBase database to construct a long non-coding RNA-miRNA-mRNA global competing endogenous RNA network and extract asthma-related differentially expressed competing endogenous RNA network. Finally, functional enrichment analysis and drug repositioning of asthma-associated differentially expressed competing endogenous RNA networks were performed to further identify key long non-coding RNAs and potential therapeutics associated with asthma. Results: This study constructed an asthma-associated competing endogenous RNA network, determined 5 key long non-coding RNAs (MALAT1, MIR17HG, CASC2, MAGI2-AS3, DAPK1-IT1) and identified 8 potential new drugs (Tamoxifen, Ruxolitinib, Tretinoin, Quercetin, Dasatinib, Levocarnitine, Niflumic Acid, Glyburide). Conclusions: The results suggested that long non-coding RNA played an important role in asthma, and these novel long non-coding RNAs could be potential therapeutic target and prognostic biomarkers. At the same time, potential new drugs for asthma treatment have been discovered through drug repositioning techniques, providing a new direction for the treatment of asthma.

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LncRNA-MEG3 functions as a competing endogenous RNA to regulate Treg/Th17 balance in patients with asthma by targeting microRNA-17/ RORγt

Cited by 112 publications

References 34 publications

Long non‑coding RNA EBLN3P promotes the recovery of the function of impaired spiral ganglion neurons by competitively binding to miR‑204‑5p and regulating TMPRSS3 expression

Long non‑coding RNA EBLN3P promotes the recovery of the function of impaired spiral ganglion neurons by competitively binding to miR‑204‑5p and regulating TMPRSS3 expression

Expression of Long Non-Coding RNAs by Human Retinal Müller Glial Cells Infected with Clonal and Exotic Virulent Toxoplasma gondii

Construction of asthma related competing endogenous RNA network revealed novel long non-coding RNAs and potential new drugs

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