Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

Maarouf, Mohamed; Chen, Biao; Chen, Yongqin David; Wang, Xuefei; Raj, Kul; Zhao, Zhonghui; Li, Shasha; Li, Yingying; Xiao, Meng; Chen, Ji‐Long

doi:10.1111/cmi.13036

Cited by 62 publications

(88 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…responses against viral infections [8]. Additionally, MIR155HG has been revealed to function as an oncogene in the progression of diverse cancers, such as pancreatic cancer, glioblastoma and laryngeal squamous cell carcinoma [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis

Song

Wang²,

Zong

2020

Bioscience Reports

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is a common airway disease characterized by an exaggerated pulmonary inflammatory response. Long noncoding MIR155 host gene (lncRNA MIR155HG) has been identified to be related to the macrophage polarization in COPD. However, the detailed function of MIR155HG in cigarette smoke (CS)-mediated COPD remains largely unknown. The expression level of MIR155HG was elevated while miR-218-5p was decreased in lung tissues of smokers without or with COPD, especially in smokers with COPD, and cigarette smoke extract (CSE)-treated human pulmonary microvascular endothelial cell (HPMECs) in a dose-and time-dependent manner. Then, functional experiments showed that MIR155HG deletion could reverse CSE exposure-induced apoptosis and inflammation in HPMECs. MiR-218-5p was confirmed to be a target of MIR155HG and rescue assay showed miR-218-5p inhibitor attenuated the inhibitory action of MIR155HG knockdown on CSE-induced HPMECs. Subsequently, miR-218-5p was found to target bromodomain containing 4 (BRD4) directly, and miR-218-5p overexpression overturned CSE-induced injury of HPMECs via regulating BRD4. Additionally, co-expression analysis indicated MIR155HG indirectly regulated BRD4 expression in HP-MECs via miR-218-5p. Thus, we concluded that MIR155HG contributed to the apoptosis and inflammation of HPMECs in smoke-related COPD by regulating miR-128-5p/BRD4 axis, providing a novel insight on the pathogenesis of COPD and a therapeutic strategy on COPD treatments.According to the prediction of DIANA-LncBaseV2 prediction program, miR-218-5p might be a potential target of MIR155HG ( Figure 3A). To verify this prediction, luciferase reporter assay was performed and we found miR-218-5p mimic transfection reduced the luciferase activity of the MIR155HG-WT reporter vector but not MIR155HG-MUT reporter vector in HPMECs ( Figure 3B). However, miR-218-5p inhibitor transfection enhanced the luciferase activity

show abstract

Section: Introductionmentioning

confidence: 99%

LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis

Song

Wang²,

Zong

2020

Bioscience Reports

View full text Add to dashboard Cite

show abstract

“…As a general rule, lncRNAs whose expression is altered by the antiviral pathways should show deregulation in response to infection with several other viruses, and/or in response to treatment with IFN and/or different PAMPs. This is the case of lncRNA TSPOAP1-AS1 (TSPOAP1 antisense RNA 1) and MIR155HG (miRNA-155 host gene), upregulated in response to infection with influenza and other viruses and by the dsRNA mimic pI:C (lncRNA TSPOAP1-AS1) [85,86]. Interestingly, lncRNA TSPOAP1-AS1 inhibits IFNβ and ISG transcription, playing a proviral role, whereas MIR155HG functions as an antiviral by inhibiting PTP1B (protein tyrosine phosphatase 1B), resulting in higher production of IFNβ and several ISGs.…”

Section: Lncrnas That Affect the Antiviral Responsementioning

confidence: 99%

LncRNAs in HCV Infection and HCV-Related Liver Disease

Unfried¹,

Fortes²

2020

IJMS

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) are transcripts with poor coding capacity that may interact with proteins, DNA, or other RNAs to perform structural and regulatory functions. The lncRNA transcriptome changes significantly in most diseases, including cancer and viral infections. In this review, we summarize the functional implications of lncRNA-deregulation after infection with hepatitis C virus (HCV). HCV leads to chronic infection in many patients that may progress to liver cirrhosis and hepatocellular carcinoma (HCC). Most lncRNAs deregulated in infected cells that have been described function to potentiate or block the antiviral response and, therefore, they have a great impact on HCV viral replication. In addition, several lncRNAs upregulated by the infection contribute to viral release. Finally, many lncRNAs have been described as deregulated in HCV-related HCC that function to enhance cell survival, proliferation, and tumor progression by different mechanisms. Interestingly, some HCV-related HCC lncRNAs can be detected in bodily fluids, and there is great hope that they could be used as biomarkers to predict cancer initiation, progression, tumor burden, response to treatment, resistance to therapy, or tumor recurrence. Finally, there is high confidence that lncRNAs could also be used to improve the suboptimal long-term outcomes of current HCC treatment options.

show abstract

“…The potential functions of differentially expressed mRNAs, miRNAs and circRNAs were anlyzed and were closely related to inflammatory response [16]. Recently, increasing studies have indicated that lncRNAs play important roles in inflammatory response [17][18][19][20]. Therefore, we proposed that lncRNAs also might participate in regulating inflammatory response during TGEV infection.…”

Section: Introductionmentioning

confidence: 99%

Identification and analysis of long non-coding RNAs that are involved in inflammatory process in response to transmissible gastroenteritis virus infection

Zhao

Wang

et al. 2019

BMC Genomics

View full text Add to dashboard Cite

Background: Transmissible gastroenteritis virus (TGEV) infection can cause acute inflammation. Long noncoding RNAs (lncRNAs) play important roles in a number of biological process including inflammation response. However, whether lncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells (IPECs) is largely unknown. Results: In this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of lncRNAs in Mock and TGEV-infected porcine intestinal epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 106 lncRNAs were differentially expressed. Many differentially expressed lncRNAs act as elements to competitively attach microRNAs (miRNAs) which target to messenger RNA (mRNAs) to mediate expression of genes that related to tolllike receptors (TLRs), NOD-like receptors (NLRs), tumor necrosis factor (TNF), and RIG-I-like receptors (RLRs) pathways. Functional analysis of the binding proteins and the up/down-stream genes of the differentially expressed lncRNAs revealed that lncRNAs were principally related to inflammatory response. Meanwhile, we found that the differentially expressed lncRNA TCONS_00058367 might lead to a reduction of phosphorylation of transcription factor p65 (p-p65) in TGEV-infected IPEC-J2 cells by negatively regulating its antisense gene promyelocytic leukemia (PML). Conclusions:The data showed that differentially expressed lncRNAs might be involved in inflammatory response induced by TGEV through acting as miRNA sponges, regulating their up/down-stream genes, or directly binding proteins.

show abstract

Identification of lncRNA‐155 encoded by MIR155HG as a novel regulator of innate immunity against influenza A virus infection

Cited by 62 publications

References 53 publications

LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis

LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis

LncRNAs in HCV Infection and HCV-Related Liver Disease

Identification and analysis of long non-coding RNAs that are involved in inflammatory process in response to transmissible gastroenteritis virus infection

Contact Info

Product

Resources

About