Long Noncoding RNA HOXA Cluster Anti-Sense RNA 2 Inhibits Mycoplasma pneumoniae-Induced Inflammation by Regulating the Nuclear Factor-KappaB Signaling Pathway

2021 ◽  
Vol 11 (11) ◽  
pp. 2262-2273
Author(s):  
Mei Feng ◽  
Chengjie Zhuo ◽  
Xuefen Zhu
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Mycoplasma Pneumoniae ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Flow Cytometric Analysis ◽  
Inflammatory Factors ◽  
Epithelial Cell Line ◽  
Inflammatory Factor ◽  
Hoxa Cluster

Mycoplasma pneumoniae (MP) is the primary cause of community-acquired lung inflammation. The MP-induced manifestations of pneumonia are associated with the release of pro-inflammatory cytokines; however, the mechanisms of MP-induced inflammation have not been fully clarified. The purpose of the present study was to determine whether long noncoding RNA HOXA cluster anti-sense RNA 2 (lncRNA HOXA-AS2) is involved in MP-induced inflammation. A model of MP-induced cellular inflammation was established using the human BEAS-2B lung epithelial cell line and lncRNA HOXA-AS2 levels were detected using reverse transcription-quantitative (RT-q) PCR. MTT and flow cytometric analysis were used to assess cell viability and apoptosis, respectively. The secretion of pro-inflammatory factors including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were measured by ELISA, and protein levels of phosho- (p-)p65 and p-NF-κB inhibitor α (p-IκBα) were detected by western blotting. The results suggest that MP infection significantly decreases the level of lncRNA HOXA-AS2 in BEAS-2B cells. lncRNA HOXA-AS2 overexpression significantly enhanced cell viability, inhibited apoptosis, decreased pro-inflammatory factor expression (TNF-α, IL-β and IL-6) and inhibited NF-κB pathway activation in MP-stimulated BEAS-2B cells. Conversely, lncRNA HOXA-AS2-knockdown resulted in the opposite effects. In conclusion, lncRNA HOXA-AS2 is involved in MP infection-induced inflammation and regulates the NF-κB signaling pathway.

scholarly journals Long noncoding RNA KCNQ1OT1 targets miRNA let-7a-5p to regulate Osteoarthritis development and progression

2021 ◽  
Author(s):  
hafiza sobia ramzan ◽  
Kashif Aziz Ahmad
Keyword(s):  
Cell Viability ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Luciferase Assay ◽  
Common Disease ◽  
Functional Roles ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Long Non Coding Rna

Background: Osteoarthritis (OA) is a common disease of the joints among old populace until today. The treatment possibilities and roles of miRNA and long non-coding RNA (lncRNA) in therapy of OA has previously been explored. However, the functional roles of Long noncoding RNA KCNQ1OT1 and miRNA let-7a-5p on Osteoarthritis development and progression remains unclear. This study aimed at investigating the influence of KCNQ1OT1 on let-7a-5p in moderation of OA development and advancement. Materials and Methods: RT-qPCR examined expression of KCNQ1OT1and let-7a-5p in cultured human primary chondrocyte cell lines. Cell transfection overexpressed or knocked down the genes and CCK-8 assay measured cell viability in the proliferation biomarkers Ki87 and PCNA. While caspase-8 and caspase-3 activity determined rate of apoptosis. Furthermore, luciferase assay analyzed the luciferase activity and western blotting analysis determined the protein expression of KCNQ1OT1 and let-7a-5p in proliferation and apoptosis biomarkers. Results: The results demonstrated that KCNQ1OT1 is upregulated in OA-mimic cells and promotes the cell viability. KCNQ1OT1 knockdown suppresses cell viability of OA cells. Furthermore KCNQ1OT1 directly binds the 3'-UTR of let-7a-5p to negatively regulate let-7a-5p expression and OA progression. While upregulated let-7a-5p abolishes the proliferation effect of KCNQ1OT1 in OA cells. Conclusion: In summary, our study provides further insights into the underlying molecular mechanisms of KCNQ1OT1 and let-7a-5p suggesting a novel therapeutic approach to OA

Ulinastatin Activated The ERK5/Mer Signaling Pathway To Promote Macrophage Efferocytosis And Ameliorate Lung Inflammation

2021 ◽  
Author(s):  
Jinju Li ◽  
Rongge Shao ◽  
Qiuwen Xie ◽  
XueKe Du
Keyword(s):  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Inflammation ◽  
Raw264.7 Cells ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Dependent Manner ◽  
Anti Inflammatory

Abstract Purpose:Ulinastatin (UTI) is an endogenous protease inhibitor with potent anti-inflammatory, antioxidant and organ protective effects. The inhibitor has been reported to ameliorate inflammatory lung injury but precise mechanisms remain unclear. Methods: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). The number of neutrophils and the phagocytosis of apoptotic neutrophils were observed by Diff- Quick method. Lung injury was observed by HE staining .BALF cells were counted by hemocytometer and concentrations of protein plus inflammatory factors were measured with a BCA test kit. During in vitro experiments, RAW264.7 cells were pretreated with UTI (1000 and 5000U/ mL), stained with CellTrackerTM Green B0DIPYTM and HL60 cells added with UV-induced apoptosis and PKH26 Red staining. The expression of ERK5\Mer related proteins was detected by western blot and immunofluorescence.Results: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). UTI treatment enhanced the phagocytotic effect of mouse alveolar macrophages on neutrophils, alleviated lung lesions, decreased the pro-inflammatory factor and total protein content of BALF and increased levels of anti-inflammatory factors. in vitro experiments ，UTI enhanced the phagocytosis of apoptotic bodies by RAW264.7 cells in a dose-dependent manner. Increased expression levels of ERK5 and Mer by UTI were shown by Western blotting and immunofluorescence.Conclusions: UTI mediated the activation of the ERK5/Mer signaling pathway, enhanced phagocytosis of neutrophils by macrophages and improved lung inflammation. The current study indicates potential new clinical approaches for accelerating the recovery from lung inflammation.

A novel long noncoding RNA FAF inhibits apoptosis via upregulating FGF9 through PI3K/AKT signaling pathway in ischemia–hypoxia cardiomyocytes

2019 ◽  
Vol 234 (12) ◽  
pp. 21973-21987 ◽  
Author(s):  
Hao‐Jie Shi ◽  
Ming‐Wei Wang ◽  
Jia‐Teng Sun ◽  
Hao Wang ◽  
Ya‐Fei Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKβ/NF-κB signaling pathway

2018 ◽  
Vol 315 (1) ◽  
pp. C52-C61 ◽  
Author(s):  
Heng-Jun Zhou ◽  
Li-Qing Wang ◽  
Duan-Bu Wang ◽  
Jian-Bo Yu ◽  
Yu Zhu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Proinflammatory Cytokines ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Tnf Α ◽  
Cord Injury

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was widely recognized to be implicated in human cancer, vascular diseases, and neurological disorders. This study was to explore the role and underlying mechanism of MALAT1 in acute spinal cord injury (ASCI). ASCI models in adult rats were established and demonstrated by a numerical decrease in BBB scores. Expression profile of MALAT1 and miR-199b following ASCI in rats and in vitro was determined using quantitative real-time PCR. RNA pull-down assays combined with RIP assays were performed to explore the interaction between MALAT1 and miR-199b. In the present study, MALAT1 expression was significantly increased (2.4-fold that of control) in the spinal cord of the rat contusion epicenter accompanied by activation of IKKβ/NF-κB signaling pathway and an increase in the level of proinflammatory cytokines TNF-α and IL-1β. Upon treatment with LPS, MALAT1 expression dramatically increased in the microglia in vitro, but knockdown of MALAT1 attenuated LPS-induced activation of MGs and TNF-α and IL-1β production. Next, we confirmed that LPS-induced MALAT1 activated IKKβ/NF-κB signaling pathway and promoted the production of proinflammatory cytokines TNF-α and IL-1β through downregulating miR-199b. More importantly, MALAT1 knockdown gradually improved the hindlimb locomotor activity of ASCI rats as well as inhibited TNF-α, IL-1β levels, and Iba-1 protein, the marker of activated microglia in injured spinal cords. Our study demonstrated that MALAT1 was dysregulated in ASCI rats and in LPS-activated MGs, and MALAT1 knockdown was expected to attenuate ASCI through repressing inflammatory response of MGs.

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