Long non-coding RNA ANRIL regulates inflammatory responses as a novel component of NF-κB pathway

Background Clostridium perfringens (C. perfringens) type C is the most common bacteria causing piglet diarrheal disease and it greatly affects the economy of the global pig industry. The spleen is an important immune organ in mammals; it plays an irreplaceable role in resisting and eradicating pathogenic microorganisms. Based on different immune capacity in piglets, individuals display the resistance and susceptibility to diarrhea caused by C. perfringens type C. Recently, long non-coding RNA (lncRNA) and mRNA have been found to be involved in host immune and inflammatory responses to pathogenic infections. However, little is known about spleen transcriptome information in piglet diarrhea caused by C. perfringens type C. Methods Hence, we infected 7-day-old piglets with C. perfringens type C to lead to diarrhea. Then, we investigated lncRNA and mRNA expression profiles in spleens of piglets, including control (SC), susceptible (SS), and resistant (SR) groups. Results As a result, 2,056 novel lncRNAs and 2,417 differentially expressed genes were found. These lncRNAs shared the same characteristics of fewer exons and shorter length. Bioinformatics analysis identified that two lncRNAs (ALDBSSCT0000006918 and ALDBSSCT0000007366) may be involved in five immune/inflammation-related pathways (such as Toll-like receptor signaling pathway, MAPK signaling pathway, and Jak-STAT signaling pathway), which were associated with resistance and susceptibility to C. perfringens type C infection. This study contributes to the understanding of potential mechanisms involved in the immune response of piglets infected with C. perfringens type C.

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Long non‐coding RNA MALAT1 sponges miR‐149 to promote inflammatory responses of LPS‐induced acute lung injury by targeting MyD88

Cell Biology International ◽

10.1002/cbin.11235 ◽

2019 ◽

Vol 44 (1) ◽

pp. 317-326 ◽

Cited By ~ 7

Author(s):

Wei‐Jun Liang ◽

Xiao‐Yuan Zeng ◽

Sha‐Li Jiang ◽

Hong‐Yi Tan ◽

Mu‐Yun Yan ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Inflammatory Responses ◽

Non Coding Rna ◽

Long Non Coding Rna

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Long non-coding RNA lncC11orf54-1 modulates neuroinflammatory responses by activating NF-κB signaling during meningitic Escherichia coli infection

Molecular Brain ◽

10.1186/s13041-021-00890-8 ◽

2022 ◽

Vol 15 (1) ◽

Author(s):

Bojie Xu ◽

Ruicheng Yang ◽

Bo Yang ◽

Liang Li ◽

Jiaqi Chen ◽

...

Keyword(s):

Escherichia Coli ◽

Nuclear Factor Kappa B ◽

Inflammatory Responses ◽

Interleukin 1 ◽

E Coli ◽

Non Coding Rna ◽

Escherichia Coli Infection ◽

Non Coding Rnas ◽

Long Non Coding Rna ◽

Pro Inflammatory Cytokines

AbstractEscherichia coli is the most common gram-negative pathogenic bacterium causing meningitis. It penetrates the blood–brain barrier (BBB) and activates nuclear factor kappa B (NF-κB) signaling, which are vital events leading to the development of meningitis. Long non-coding RNAs (lncRNAs) have been implicated in regulating neuroinflammatory signaling, and our previous study showed that E. coli can induce differential expression of lncRNAs, including lncC11orf54-1, in human brain microvascular endothelial cells (hBMECs). The hBMECs constitute the structural and functional basis for the BBB, however, it is unclear whether lncRNAs are involved in the regulation of inflammatory responses of hBMECs during meningitic E. coli infection. In this study, we characterized an abundantly expressed lncRNA, lncC11orf54-1, which was degraded by translocated coilin to produce mgU2-19 and mgU2-30 in hBMECs during E. coli infection. Functionally, lncC11orf54-1-originated non-coding RNA mgU2-30 interacted with interleukin-1 receptor-associated kinase 1 (IRAK1) to induce its oligomerization and autophosphorylation, thus promoting the activation of NF-κB signaling and facilitating the production of pro-inflammatory cytokines. In summary, our study uncovers the involvement of lncC11orf54-1 in IRAK1–NF-κB signaling, and it functions as a positive regulator of inflammatory responses in meningitic E. coli-induced neuroinflammation, which may be a valuable therapeutic and diagnostic target for bacterial meningitis.

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Long non-coding RNA PVT1 can regulate the proliferation and inflammatory responses of rheumatoid arthritis fibroblast-like synoviocytes by targeting microRNA-145-5p

Human Cell ◽

10.1007/s13577-020-00419-6 ◽

2020 ◽

Vol 33 (4) ◽

pp. 1081-1090

Author(s):

Jiajun Tang ◽

Shiyu Yi ◽

Yi Liu

Keyword(s):

Rheumatoid Arthritis ◽

Inflammatory Responses ◽

Non Coding Rna ◽

Long Non Coding Rna ◽

Fibroblast Like Synoviocytes

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Epigenetic Programming of Cancer-Related Inflammation byncRNA Rheostat: Impact on Tumor Directed Immune Therapies

10.20944/preprints202109.0148.v1 ◽

2021 ◽

Author(s):

Roshan Roy ◽

Uttam Sharma ◽

Rakhi Yadav ◽

Manjit Kaur Rana ◽

Ashok Sharma ◽

...

Keyword(s):

Inflammatory Responses ◽

Tumor Development ◽

Cellular Level ◽

Cellular Processes ◽

Epigenetic Programming ◽

Non Coding Rna ◽

Immune Therapies ◽

Covalent Modifications ◽

Living Organisms ◽

Long Non Coding Rna

Accumulating evidences demonstrate that the host genome's epigenetic modificationsare essential for living organisms to adapt extreme conditions.DNA methylation, covalent modifications of histone, andinter-association of non-coding RNAs facilitate the cellular manifestation ofepigenetic changes in the genome. Out of various factors involved in the epigenetic programming of the host, miRNA (microRNA) and LncRNA (Long non-coding RNA) are new generationnon-coding molecules that influence a variety of cellular processes like immunity, cellular differentiation, and tumor development. During tumor development, temporal changes in miRNA/LncRNA rheostat influence sterile inflammatory responses accompanied by the changes in the carcinogenic signalling in the host. At the cellular level, this is manifested by the up-regulation of Inflammasome and inflammatory pathways, which promotes cancer-related inflammation. In view of this, we discuss the potential of lncRNA and miRNA directed interventions in regulating inflammation and tumor development in the host.

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P2666Endothelial microvesicles-incorporated long non-coding RNA PUNISHER regulates inflammatory responses in THP1 recipient cells

European Heart Journal ◽

10.1093/eurheartj/ehy565.p2666 ◽

2018 ◽

Vol 39 (suppl_1) ◽

Author(s):

Q Li ◽

Y Y Liu ◽

G Nickenig ◽

N Werner ◽

F Jansen

Keyword(s):

Inflammatory Responses ◽

Non Coding Rna ◽

Long Non Coding Rna

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A reduced level of the long non-coding RNA SNHG8 activates the NF-kappaB pathway by releasing functional HIF-1alpha in a hypoxic inflammatory microenvironment

10.21203/rs.3.rs-850529/v1 ◽

2021 ◽

Author(s):

Chenxin Wang ◽

Qiaolin Yang ◽

Yineng Han ◽

Hao Liu ◽

Yue Wang ◽

...

Keyword(s):

Rna Sequencing ◽

Inflammatory Responses ◽

Compressive Force ◽

Periodontal Tissue ◽

Non Coding Rna ◽

Long Non Coding Rna ◽

Periodontal Tissue Remodeling

Abstract Background A series of biochemical responses, including hypoxia and aseptic inflammation, occur in periodontal ligament cells (PDLCs) during periodontal tissue remodeling of orthodontic tooth movement (OTM). However, the role of long non-coding RNA (lncRNA) in these responses is still largely unknown. We investigated the role of the lncRNA SNHG8 in hypoxic and inflammatory responses during OTM, and explored the underlying mechanisms. Methods The expression pattern of SNHG8, and hypoxic and inflammatory responses under compressive force, were analyzed by qRT-PCR, immunohistochemistry, and western blotting, in vivo and in vitro. The effect of overexpression or knockdown of SNHG8 on the nuclear factor-kappaB (NF-κB) pathway was evaluated. RNA sequencing was performed for mechanistic analysis. The interaction between SNHG8 and hypoxia-inducible factor (HIF)-1α was studied using catRAPID, RNA immunoprecipitation, and RNA pulldown assays. The effect of the SNHG8–HIF-1α interaction on the NF-κB pathway was determined by western blotting. Results The NF-κB pathway was activated, and HIF-1α release was stabilized, in PDLCs under compressive force as well as in OTM model rats. The SNHG8 level markedly decreased both in vivo and in vitro. Overexpression of SNHG8 decreased the expression levels of inflammatory cytokines, the phosphorylation of p65, and the degradation of IκBα in PDLCs, whereas knockdown of SNHG8 reversed these effects. Mechanically, RNA sequencing showed that differentially expressed genes were enriched in cellular response to hypoxia after SNHG8 overexpression. SNHG8 binds to HIF-1α, thus preventing HIF-1 from activating downstream genes, including those related to the NF-κB pathway. Conclusion SNHG8 binds to HIF-1α. During OTM, the expression of SNHG8 dramatically decreased, releasing free functional HIF-1α and activating the downstream NF-κB pathway. These data suggest a novel lncRNA-regulated mechanism during periodontal tissue remodeling in OTM.

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