scholarly journals Extended lifespan of bronchial epithelial cells maintains normal cellular phenotype and transcriptome integrity

2021 ◽  
Vol 7 (1) ◽  
pp. 00254-2020
Author(s):  
Jonathan O'Loughlin ◽  
Robert J. Hall ◽  
Sangita Bhaker ◽  
Michael A. Portelli ◽  
Amanda Henry ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cell Attachment ◽  
Bronchial Epithelial Cells ◽  
Polycomb Group ◽  
Proliferative Potential ◽  
Polycomb Group Protein ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition

Genetic studies have identified several epithelial-derived genes associated with airway diseases. However, techniques used to study gene function frequently exceed the proliferative potential of primary human bronchial epithelial cells (HBECs) isolated from patients. Increased expression of the polycomb group protein BMI-1 extends the lifespan of HBECs while maintaining cell context plasticity. Herein we aimed to assess how BMI-1 expression impacted cellular functions and global mRNA expression. HBECs from six donors were transduced with lentivirus containing BMI-1 and cells were characterised, including by RNA sequencing and impedance measurement. BMI-1-expressing HBECs (B-HBECs) have a proliferative advantage and show comparable in vitro properties to low passage primary HBECs, including cell attachment/spreading and barrier formation. The B-HBEC mRNA signature was modestly different to HBECs, with only 293 genes differentially expressed (5% false discovery rate). Genes linked to epithelial mesenchymal transition and cell cycle were enriched in B-HBECs. We investigated the expression of genes implicated in asthma from genetic and expression studies and found that 97.6% of genes remained unaltered. We have shown that increased BMI-1 expression in HBECs delays lung epithelial cell senescence by promoting cell cycle progression and highlighted the flexible utility for B-HBECs as an important platform for studying airway epithelial mechanisms.

scholarly journals Ionizing radiation induces epithelial–mesenchymal transition in human bronchial epithelial cells

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Bo Tang ◽  
Yue Xi ◽  
Fengmei Cui ◽  
Jin Gao ◽  
Huiqin Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Ionizing Radiation ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Migration Ability ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Potential Biomarker

Abstract Objective: The present study aimed to analyze the mechanism by which long-term occupational exposure of workers to low-dose ionizing irradiation induces epithelial–mesenchymal transition (EMT) of the human bronchial epithelial cells using transcriptome profiling. Methods: RNA-seq transcriptomics was used to determine gene expression in blood samples from radiation-exposed workers followed by bioinformatics analysis. Normal bronchial epithelial cells (16HBE) were irradiated for different durations and subjected to immunofluorescence, Western blotting, scratch healing, and adhesion assays to detect the progression of EMT and its underlying molecular mechanisms. Results: Transcriptomics revealed that exposure to ionizing radiation led to changes in the expression of genes related to EMT, immune response, and migration. At increased cumulative doses, ionizing radiation-induced significant EMT, as evidenced by a gradual decrease in the expression of E-cadherin, increased vimentin, elevated migration ability, and decreased adhesion capability of 16HBE cells. The expression of fibronectin 1 (FN1) showed a gradual increase with the progression of EMT, and may be involved in EMT. Conclusion: Ionizing radiation induces EMT. FN1 may be involved in the progression of EMT and could serve as a potential biomarker for this process.

scholarly journals Airway Epithelial Repair by a Prebiotic Mannan Derived from Saccharomyces cerevisiae

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Christie F. Michael ◽  
Christopher M. Waters ◽  
Kim S. LeMessurier ◽  
Amali E. Samarasinghe ◽  
Chi Y. Song ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Wound Repair ◽  
Epithelial Mesenchymal Transition ◽  
Bronchial Epithelial Cells ◽  
Current Therapy ◽  
Airway Epithelial ◽  
Coated Pits ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Mannose Receptors

In asthmatic airways, repeated epithelial damage and repair occur. No current therapy directly targets this process. We aimed to determine the effects of mannan derived from S. cerevisiae (SC-MN) on airway epithelial wound repair, in vitro. The presence of functional mannose receptors in bronchial epithelial cells was shown by endocytosis of colloidal gold-Man BSA via clathrin-coated pits in 16HBE cells. In primary normal human bronchial epithelial cells (NHBEC), SC-MN significantly facilitated wound closure. Treatment with SC-MN stimulated cell spreading as indicated by a significant increase in the average lamellipodial width of wound edge 16HBE cells. In addition, NHBEC treated with SC-MN showed increased expression and activation of Krüppel-like factors (KLFs) 4 and 5, transcription factors important in epithelial cell survival and regulation of epithelial-mesenchymal transition. We conclude that SC-MN facilitates wound repair in human bronchial epithelium, involving mannose receptors.

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