scholarly journals circ_0038467 promotes PM2.5-induced bronchial epithelial cell dysfunction

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 854-863
Author(s):  
Xuan Jin ◽  
Li Wang ◽  
Mingzhu Yang
Keyword(s):  
Epithelial Cell ◽  
Western Blot ◽  
Bronchial Epithelial Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Epithelial Cell Line ◽  
Binding Interaction ◽  
Bronchial Epithelial ◽  
Lung Dysfunction

Abstract Purpose This study was to explore the toxicological mechanisms by which PM2.5 causes lung dysfunction. Methods The expression of circ_0038467 and miR-138-1-3p in PM2.5-induced human bronchial epithelial cell line BEAS-2B was detected by RT-qPCR. The effects of circ_0038467 and miR-138-1-3p on proliferation, apoptosis, and inflammatory cytokines (IL-6 and IL-8) in PM2.5-induced BEAS-2B were determined using cell counting kit-8, flow cytometry, western blot, and enzyme-linked immunosorbent assay, respectively. The levels of nuclear factor kappa B (NF-κB) pathway-related protein were also analyzed by western blot. The binding interaction between circ_0038467 and miR-138-1-3p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay and pull-down assay. Results circ_0038467 expression was increased by PM2.5 treatment in BEAS-2B cells in time- and dose-dependent methods, and knockdown of circ_0038467 reversed PM2.5-triggered BEAS-2B cell death and inflammatory response. miR-138-1-3p was decreased by PM2.5 treatment, and restoration of miR-138-1-3p attenuated PM2.5-induced BEAS-2B cell injury. In a mechanical study, we found circ_0038467 directly bound to miR-138-1-3p, and further rescue experiments exhibited miR-138-1-3p inhibition partially overturned the regulatory functions of circ_0038467 knockdown in PM2.5-induced BEAS-2B cells. Conclusion circ_0038467 provided a potential therapeutic strategy for future clinic intervention in air pollution-triggered lung dysfunction.

scholarly journals Mesenchymal stem cell-originated exosomal lncRNA HAND2-AS1 impairs rheumatoid arthritis fibroblast-like synoviocyte activation through miR-143-3p/TNFAIP3/NF-κB pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yuhua Su ◽  
Yajing Liu ◽  
Chao Ma ◽  
Chunxiao Guan ◽  
Xiufen Ma ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Western Blot ◽  
Tumor Necrosis ◽  
Cell Counting ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Binding Interaction ◽  
Necrosis Factor

Abstract Background Long non-coding RNA heart and neural crest derivatives expressed 2-antisense RNA 1 (HAND2-AS1) was found to be elevated in rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs). However, whether HAND2-AS1 functions as an exosomal lncRNA related to mesenchymal stem cells (MSCs) in RA progression is unknown. Methods The expression of HAND2-AS1, microRNA (miR)-143-3p, and tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) was detected using quantitative real-time polymerase chain reaction and Western blot. Cell proliferation, apoptosis, migration, and invasion were detected using cell counting kit-8, flow cytometry, and wound healing and transwell assays. The levels of tumor necrosis factor-α (TNF-α) and interleukins (IL)-6 were analyzed using enzyme-linked immunosorbent assay. The level of phosphorylated-p65 was examined by Western blot. The binding interaction between miR-143-3p and HAND2-AS1 or TNFAIP3 was confirmed by the dual-luciferase reporter and RIP assays. Exosomes were isolated by ultracentrifugation and qualified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. Results HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. Mechanistically, HAND2-AS1 directly sponged miR-143-3p and positively regulated TNFAIP3 expression, the target of miR-143-3p. Moreover, the effects of HAND2-AS1 on RA-FLSs were partially attenuated by miR-143-3p upregulation or TNFAIP3 knockdown. HAND2-AS1 could be packaged into hMSC-derived exosomes and absorbed by RA-FLSs, and human MSC-derived exosomal HAND2-AS1 also repressed above malignant biological behavior of RA-FLSs. Conclusion MSC-derived exosomes participated in the intercellular transfer of HAND2-AS1 and suppressed the activation of RA-FLSs via miR-143-3p/TNFAIP3/NF-κB pathway, which provided a novel insight into the pathogenesis and treatment of RA.

Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line

2004 ◽  
Vol 286 (4) ◽  
pp. L777-L785 ◽  
Author(s):  
Kei Takamura ◽  
Yasuyuki Nasuhara ◽  
Motoko Kobayashi ◽  
Tomoko Betsuyaku ◽  
Yoko Tanino ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cell ◽  
Cell Line ◽  
Nuclear Translocation ◽  
Bronchial Epithelial Cell ◽  
Inhibitory Effect ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Transcriptional Level ◽  
Bronchial Epithelial

Retinoic acid (RA) is known to accelerate wound healing and induce cell differentiation. All- trans RA (ATRA) exerts its effect by binding retinoic acid receptors, which are members of the nuclear receptor family. We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-κB. We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. ATRA and its stereodimer 9- cis retinoic acid (9- cis RA) inhibited IL-4-induced release of eotaxin at 10-6M by 78.0 and 52.0%, respectively ( P < 0.05). ATRA and 9- cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10-6M by 52.3 and 53.5%, respectively ( P < 0.05). In contrast, neither ATRA nor 9- cis RA had any effects on TNF-α-induced eotaxin production. In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Interestingly, ATRA had no effects on IL-4-induced tyrosine phosphorylation, nuclear translocation, or DNA binding activity of STAT6. Activating protein-1 was not involved in ATRA-mediated transrepression of eotaxin with IL-4 stimulation. The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. These findings raise the possibility that RA may reduce eosinophilic airway inflammation, one of the prominent pathological features of allergic diseases such as bronchial asthma.

scholarly journals A Comparative Study on the Model of PM2.5 Direct or Indirect Interaction with Bronchial Epithelial Cells.

2021 ◽  
Author(s):  
Yan Wang ◽  
Xin Zuo ◽  
Fuyang Jiang ◽  
Lin Hou ◽  
Qiyue Jiang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Damage ◽  
Direct Interaction ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Exposure Model ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
The Impact

Abstract The impact of PM2.5 on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM2.5 direct interaction with epithelia, macrophages that engulf PM2.5 may also influence the function of epithelial cells. However, among the toxic researches of PM2.5, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM2.5. In this present research, PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model, while the contrast is to indirect stimulation model, which takes advantage of transwell co-culture system to carry out that PM2.5 is promptly contacted with macrophages rather than BEAS-2B. By comparing these two modes of interaction, we determined the viability of BEAS-2B and mRNA and/or protein expression profile of transcription factors Nrf2,NF-kB and according inflammatory indicators, with a view to evaluating the effects of different interaction modes of PM2.5 on epithelial cell damage in vitro. We have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while strengthen the inflammation response.

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