Transcriptome analysis identifies the potential roles of long non‐coding RNAs during parainfluenza virus infection

Wu, Haoming; Yao, Ran-Ran; Yu, Shuang-Shuang; Chen, Hongyan; Cai, Juan; Peng, Shengnan; Pang, Xuewen; Sun, Xiuyuan; Zhang, Jun

doi:10.1002/1873-3468.13166

Cited by 4 publications

(6 citation statements)

References 47 publications

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“…Then the expression pattern of LINC02605 was detected upon virus infection. Consistent with the microarray data and our previous studies (21), LINC02605 was induced by RNA virus (Sendai virus) in THP1 cells (Figure 1A), Hela cells (Supplementary Information, Figure S2A) and HEK293T cells (Figure 1B). Besides, LINC02605 was also up-regulated by another RNA virus (VSV) (Figure 1B), DNA virus HSV-1 and DNA virus mimics poly (dA:dT) (Figure 1C).…”

Section: Linc02605 Is Induced By Virus Infection and Type I Ifn Stimulationsupporting

confidence: 91%

“…In order to gain comprehensive understandings of lncRNAs that may be involved in innate immune regulation, Arraystar LncRNA microarrays were used to screen the expression profiles of lncRNAs in HEK293T cells preand post-Sendai viral infection. Among the differential expressed lncRNAs upon viral infection, LINC02605 is up-regulated manifestly and is a potential regulator in antiviral immune response (21). In this study, we systemically studied the expression, functions, mechanism of actions of LINC02605 in antiviral immune response.…”

Section: Discussionmentioning

confidence: 99%

“…Previously, in order to screen potential novel regulators in RNA virus-induced signaling pathway, by microarray analysis, LINC02605 is identified as a candidate regulator that may be involved in modulating antiviral innate immune response (21). In this study, we aimed to systematically investigate the functions and possible mechanisms of LINC02605 in antiviral innate immune response.…”

Section: Linc02605 Is Induced By Virus Infection and Type I Ifn Stimulationmentioning

confidence: 99%

“…To obtain potential novel regulators in RNA virus induced innate immune signaling, lncRNA chip was screened. In our previous study, LINC02605 is identified as a potential candidate (21). Here, we comprehensively studied the functions and mechanisms of actions of LINC02605 in innate immune signaling.…”

Section: Introductionmentioning

confidence: 99%

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Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

Yao

et al. 2021

Front. Immunol.

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Non-coding RNAs represent a class of important regulators in immune response. Previously, LINC02605 was identified as a candidate regulator in innate immune response by lncRNA microarray assays. In this study, we systematically analyzed the functions and the acting mechanisms of LINC02605 in antiviral innate immune response. LINC02605 was up-regulated by RNA virus, DNA virus, and type I IFNs in NF-κB and Jak-stat dependent manner. Overexpression of LINC02605 promotes RNA virus-induced type I interferon production and inhibited viral replication. Consistently, knockdown of LINC02605 resulted in reduced antiviral immune response and increased viral replication. Mechanistically, LINC02605 released the inhibition of hsa-miR-107 on the expression of phosphatase and tensin homolog (PTEN). By microRNA mimics and inhibitors, hsa-miR-107 was demonstrated to not only inhibit PTEN’s expression but also negatively regulate the antiviral immune response. Knockdown of LINC02605 led to the reduction of PTEN expression both in mRNA and protein levels. Overexpression of LINC02605 had an opposite impact. Moreover, LINC02605 attenuated the serine 97 phosphorylation level of interferon regulatory factor 3 (IRF3) by promoting PTEN expression. Nucleoplasmic fragmentation assay showed that knocking down LINC02605 inhibited the nuclear translocation of IRF3, rendering the host cells more susceptible to viral invasion, while overexpression showed opposite effects. Therefore, LINC02605 is an induced lncRNA by viral infection and plays a positive feedback in antiviral immune response through modulating the nuclear translocation of IRF3.

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Section: Linc02605 Is Induced By Virus Infection and Type I Ifn Stimulationsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Linc02605 Is Induced By Virus Infection and Type I Ifn Stimulationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

Yao

et al. 2021

Front. Immunol.

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“…Therefore, this SeV‐induced lncRNA was reported as a positive regulator in defence against this virus. 70 Also, lnc‐MxA, MxA mRNAs and lnc‐Lsm3b were significantly increased in SeV‐infected cells. Lnc‐MxA facilitates the replication of SeV by interfering with the activation of IFN‐β transcription, 65 while lnc‐Lsm3b acts as a decoy for RIG‐I and prevents downstream signalling; therefore, lnc‐Lsm3b can restrict late antiviral response to SeV‐infected mice in a feedback manner to maintain immune homeostasis.…”

Section: Long Noncoding Rnasmentioning

confidence: 92%

Long noncoding RNAs in respiratory viruses: A review

Kesheh

Mahmoudvand

Shokri

2021

Reviews in Medical Virology

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Long noncoding RNAs (lncRNAs) are defined as RNA molecules longer than 200 nucleotides that can regulate gene expression at the transcriptional or post‐transcriptional levels. Both human lncRNAs and lncRNAs encoded by viruses can modulate the expression of host genes which are critical for viral replication, latency, activation of signalling pathways, cytokine and chemokine production, RNAi processing, expression of interferons (IFNs) and interferon‐stimulated genes (ISGs). Studies on lncRNAs as key regulators of host‐virus interactions may give new insights into therapeutic strategies for the treatment of related diseases. This current review focuses on the role of lncRNAs, and their interactions with respiratory viruses including influenza A virus (IAV), respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2).

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Insight into mechanisms of pig lncRNA FUT3-AS1 regulating E. coli F18-bacterial diarrhea

Fan

Jin

et al. 2022

PLoS Pathog

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Escherichia coli F18 is a common conditional pathogen that is associated with a variety of infections in humans and animals. LncRNAs have emerged as critical players in pathogen infection, but their role in the resistance of the host to bacterial diarrhea remains unknown. Here, we used piglets as animal model and identified an antisense lncRNA termed FUT3-AS1 as a host regulator related to E. coli F18 infection by RNA sequencing. Downregulation of FUT3-AS1 expression contributed to the enhancement of E. coli F18 resistance in IPEC-J2 cells. FUT3-AS1 knockdown reduced FUT3 expression via decreasing the H4K16ac level of FUT3 promoter. Besides, the FUT3-AS1/miR-212 axis could act as a competing endogenous RNA to regulate FUT3 expression. Functional analysis demonstrated that target FUT3 plays a vital role in the resistance of IPEC-J2 cells to E. coli F18 invasion. A Fut3-knockout mice model was established and Fut3-knockout mice obviously improved the ability of resistance to bacterial diarrhea. Interestingly, FUT3 could enhance E. coli F18 susceptibility by activating glycosphingolipid biosynthesis and toll-like receptor signaling which are related to receptor formation and immune response, respectively. In summary, we have identified a novel biomarker FUT3-AS1 that modulates E. coli F18 susceptibility via histone H4 modifications or miR-212/FUT3 axis, which will provide theoretical guidance to develop novel strategies for combating bacterial diarrhea in piglets.

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Transcriptome analysis identifies the potential roles of long non‐coding RNAs during parainfluenza virus infection

Cited by 4 publications

References 47 publications

Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

Interferon-Inducible LINC02605 Promotes Antiviral Innate Responses by Strengthening IRF3 Nuclear Translocation

Long noncoding RNAs in respiratory viruses: A review

Insight into mechanisms of pig lncRNA FUT3-AS1 regulating E. coli F18-bacterial diarrhea

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