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

2019 ◽  
Vol 44 (1) ◽  
pp. 317-326 ◽  
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

scholarly journals Long non-coding RNA (lncRNA): A potential therapeutic target in acute lung injury

2021 ◽  
Author(s):  
Almaz Zaki ◽  
M Shadab Ali ◽  
Vijay Hadda ◽  
Syed Mansoor Ali ◽  
Anita Chopra ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Therapeutic Target ◽  
Potential Therapeutic Target ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA CHRF accelerates LPS-induced acute lung injury through microRNA-146a/Notch1 axis

2021 ◽  
Vol 9 (16) ◽  
pp. 1299-1299
Author(s):  
Shu Luo ◽  
Xuefeng Ding ◽  
Shiqiao Zhao ◽  
Tianyi Mou ◽  
Ruixiu Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Analyses of long non-coding RNA and mRNA profiling in the spleen of diarrheic piglets caused by Clostridium perfringens type C

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5997 ◽  
Author(s):  
Zunqiang Yan ◽  
Xiaoyu Huang ◽  
Wenyang Sun ◽  
Qiaoli Yang ◽  
Hairen Shi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Clostridium Perfringens ◽  
Diarrheal Disease ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Mapk Signaling ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Type C ◽  
Long Non Coding Rna

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.

scholarly journals LncRNA HOTAIR Increases Inflammatory Responses by Activating NF-κB Pathway in LPS-Induced Acute Lung Injury

2020 ◽  
Author(s):  
XiaoMei Huang ◽  
ZeXun Mo ◽  
YuJun Li ◽  
Hua He ◽  
KangWei Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Noncoding Rna ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
A549 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Lncrna Hotair

Abstract Background Nuclear factor kappa-B (NF-κB) activation increased the expression of cytokines and further lead to lung injury was considered the main mechanism of acute lung injury (ALI). Here, we focus on exploring the potential regulatory mechanism between long noncoding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) and NF-κB on LPS-induced ALI. Methods A549 cells were then divided into 4 groups: HOTAIR group, NC group, si-HOTAIR group and si-NC group. These 4 groups were then treated with 1μg/mL lipopolysaccharides (LPS) or without LPS at 37°C for 24 h. The expression level of cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) and LncRNA HOTAIR were evaluated by quantitative Real Time Polymerase Chain Reaction (qRT-PCR) and Enzyme-linked immunosorbent assay (ELISA). Western Blot analysis was adopted for evaluating the level of p-IκBα/IκBα and p-p65/p65. Nuclear translocation of p65 was observed by immunofluorescence staining. Results qRT-PCR and ELISA assay showed that the expression of cytokines (IL-1β, IL-6 and TNF-α) and inflammatory gene HOTAIR was remarkably increased with LPS treatment (p < 0.01). Over-expression of HOTAIR significantly increased the expression of cytokines (including IL-1β, IL-6 and TNF-α) and NF-κB pathway associated proteins (including p-IκBα/IκBα and p-p65/p65), while knockdown of HOTAIR had the opposite effect (p < 0.01). The immunofluorescence assay showed that the level of p65 in the nucleus was significantly higher in the HOTAIR group and significantly lowers in the si-HOTAIR group (p < 0.01). Conclusion HOTAIR may play a pro-inflammatory response through NF-κB pathway in LPS-induced ALI, which may provide a perspective for further understanding the pathogenic mechanism of ALI.

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