scholarly journals Identification of abnormally expressed lncRNAs induced by PM2.5 in human bronchial epithelial cells

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Xing Li ◽  
Mengning Zheng ◽  
Jinding Pu ◽  
Yumin Zhou ◽  
Wei Hong ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Western Blot ◽  
Mrna Expression ◽  
Microarray Analysis ◽  
Cell Apoptosis ◽  
Expression Profiles ◽  
Bronchial Epithelial Cells ◽  
Dependent Manner ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

To investigate the effect of stimulation of human bronchial epithelial cells (HBECs) by arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5 (WSPM2.5) on the expression of long non-coding RNAs (lncRNAs) in order to find new therapeutic targets for treatment of chronic obstructive pulmonary disease (COPD). HBECs were exposed to TAPM2.5 and WSPM2.5 at a series of concentrations. The microarray analysis was used to detect the lncRNA and mRNA expression profiles. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and gene ontology (GO) enrichment were conducted to analyze the differentially expressed lncRNAs and mRNAs. Quantitative real-time PCR (qRT-PCR) was performed to confirm the differential expression of lncRNAs. Western blot was performed to study the expression of autophagy and apoptosis-associated proteins. Flow cytometry was used to detect the apoptotic cells. The results indicated that fine particulate matter (PM2.5)-induced cell damage of HBECs occurred in a dose-dependent manner. The microarray analysis indicated that treatment with TAPM2.5 and WSPM2.5 led to the alteration of lncRNA and mRNA expression profiles. LncRNA maternally expressed gene 3 (MEG3) was significantly up-regulated in HBECs after PM2.5 treatment. The results of Western blot showed that PM2.5 induced cell apoptosis and autophagy by up-regulating apoptosis-associated gene, caspase-3, and down-regulating autophagy-associated markers, Bcl-2 and LC3 expression. In addition, we demonstrated that TAPM2.5 and WSPM2.5 accelerated apoptosis of human bronchial (HBE) cells, silencing of MEG3 suppressed apoptosis and autophagy of HBE cells. These findings suggested that the lncRNA MEG3 mediates PM2.5-induced cell apoptosis and autophagy, and probably through regulating the expression of p53.

scholarly journals STING Mediates Cytosolic Dna-Induced Muc5ac Mrna Expression in Human Bronchial Epithelial Cells

2020 ◽  
Author(s):  
Masaya Ohta ◽  
Yutaka Nishida ◽  
Hisako Yagi ◽  
Aikira Aizawa ◽  
Takahito Oyanagi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
Cell Types ◽  
Bronchial Epithelial Cells ◽  
Epithelial Cell Line ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Dna Sensing ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Abstract Background: Non-autologous and autologous cytosolic DNA are recognized as danger signals by cytoplasmic sensor molecules that activate signal-transduction pathways. An important molecule in cytosolic DNA sensing is stimulator of interferon genes (STING), an endoplasmic reticulum protein activated by cyclic GMP–AMP (cGAMP) produced in response to cytosolic DNA. STING is important for innate immune responses to cytosolic DNA in immune cells; however, knowledge about its role in bronchial epithelial cells is limited. Methods: We stimulated NCI-H292 cells with poly(dA:dT) and silenced STING and other regulatory proteins, and then determined MUC5AC mRNA expression levels. Results: Cytosolic DNA increased the expression of a major respiratory mucin protein, MUC5AC, in the human respiratory epithelial cell line NCI-H292 in a STING-dependent manner. Introducing poly(dA:dT) into the cytoplasm induced MUC5AC and interferon-β (IFNβ) expression. Silencing STING by RNA interference decreased poly(dA:dT)-induced MUC5AC mRNA expression but increased IFN-β mRNA levels. Furthermore, cGAMP treatment increased MUC5AC expression but not IFN-β expression. In contrast, silencing retinoic acid-inducible gene-I (RIG-I), which is a component of a different nucleic acid-sensing system, suppressed poly(dA:dT)-induced IFN-β expression and increased MUC5AC expression. Conclusions: Unlike its role in other cell types, in human bronchial epithelial cells, STING is central to cytosolic DNA-induced MUC5AC expression, whereas IFN-β expression is dependent on RIG-I. Our data indicate a functional interaction between the STING and RIG-I pathways, suggesting the existence of intricate and cell-specific cytosolic DNA-sensing systems.

Aspergillus Fumigatus Extract Suppresses the mRNA Expression of the IP-10 in Human Bronchial Epithelial Cells

2014 ◽  
Vol 151 (1_suppl) ◽  
pp. P248-P248
Author(s):  
Bharat Bhushan ◽  
James E. Norton ◽  
Dave Gupta ◽  
Quen Sha ◽  
James W. Schroeder ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Aspergillus Fumigatus ◽  
Mrna Expression ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Microarray analysis uncovers retinoid targets in human bronchial epithelial cells

Oncogene ◽  
2003 ◽  
Vol 22 (31) ◽  
pp. 4924-4932 ◽  
Author(s):  
Yan Ma ◽  
Petra H Koza-Taylor ◽  
Debra A DiMattia ◽  
Lynn Hames ◽  
Haoning Fu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Microarray Analysis ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Feedlot dust stimulation of interleukin-6 and -8 requires protein kinase Cε in human bronchial epithelial cells

2007 ◽  
Vol 293 (5) ◽  
pp. L1163-L1170 ◽  
Author(s):  
Todd A. Wyatt ◽  
Rebecca E. Slager ◽  
Jane DeVasure ◽  
Brent W. Auvermann ◽  
Michael L. Mulhern ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Cell Line ◽  
Bronchial Epithelial Cells ◽  
Dominant Negative ◽  
Dependent Manner ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Dust Extract

Individuals exposed to dusts from concentrated animal feeding operations report increased numbers of respiratory tract symptoms, and bronchoalveolar lavage samples from such individuals demonstrate elevated lung inflammatory mediators, including interleukin (IL)-8 and IL-6. We previously found that exposure of bronchial epithelial cells to hog barn dusts resulted in a protein kinase C (PKC)-dependent increase in IL-6 and IL-8 release. We hypothesized that cattle feedlot dusts would also generate bronchial epithelial interleukin release in vitro. To test this, we used interleukin ELISAs and direct PKC isoform assays. We found that a dust extract from cattle feedlots [feedlot dust extract (FLDE)] augments PKC activity of human bronchial epithelial cells in vitro. A 5–10% dilution of FLDE stimulated a significant release of IL-6 and IL-8 at 6–24 h in a PKC-dependent manner vs. control medium-treated cells. An increase in PKCα activity was observed with 1 h of FLDE treatment, and PKCε activity was elevated at 6 h of FLDE exposure. The PKCα inhibitor, Gö-6976, did not inhibit FLDE-stimulated IL-8 and IL-6 release. However, the PKCε inhibitor, Ro 31-8220, effectively inhibited FLDE-stimulated IL-8 and IL-6 release. Inhibition of FLDE-stimulated IL-6 and IL-8 was confirmed in a dominant-negative PKCε-expressing BEAS-2B cell line but not observed in a PKCα dominant negative BEAS-2B cell line. These data support the hypothesis that FLDE exposure stimulates bronchial epithelial IL-8 and IL-6 release via a PKCε-dependent pathway.

scholarly journals Changes in microRNA and mRNA Expression with Differentiation of Human Bronchial Epithelial Cells

2013 ◽  
Vol 49 (3) ◽  
pp. 384-395 ◽  
Author(s):  
Asuncion Martinez-Anton ◽  
Milena Sokolowska ◽  
Steven Kern ◽  
A. Sally Davis ◽  
Sara Alsaaty ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mrna Expression ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial
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