Azhar, Mizan Adilah (2022) The Effects of Soluble TNF-Related Apoptosis-Inducing Ligand (TRAIL) on Epithelial-Mesenchymal Transition (EMT) Markers Expression in Human Bronchial Epithelial Cells. [Project Paper] (Submitted)
![[img]](http://psaspb.upm.edu.my/style/images/fileicons/text.png) |
Text
FPSK2 2022 4.pdf Download (1MB) |
Abstract
Respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD) are among the primary causes of mortality and morbidity worldwide. Respiratory diseases are characterised by chronic airway inflammation and structural alterations in the airway wall, known as airway remodelling. Epithelial-mesenchymal transition (EMT) has been implicated in the dysregulated epithelial wound repair that contributes to airway remodelling. EMT results in epithelial cells lining the airway to become activated and progressively acquiring mesenchymal features. Thus, epithelial markers such as E-cadherin are lost, while mesenchymal markers such as N-cadherin are gained. Increasing evidence has suggested an association between airway remodelling and a molecule called tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). High TRAIL levels and expression have been reported in patients with asthma and COPD. Even so, it is presently unclear whether soluble TRAIL could directly contribute to the induction of bronchial EMT in airway remodelling. It is hypothesised that soluble TRAIL promotes the expression of key EMT markers in human bronchial epithelial cells. Objective: This study aims to investigate the ability of soluble TRAIL to induce bronchial EMT in vitro. Methodology: Normal human bronchial epithelial cells (BEAS-2B) were treated with increasing concentrations of soluble TRAIL (1, 5, 10, 50 ng/mL) for 48 h. The cytotoxicity of soluble TRAIL were determined by MTT assay. The expression of E-cadherin and N-cadherin, key markers of EMT were assessed by Western blotting. Results: TRAIL-treated BEAS-2B cells showed no significant changes (P<0.05) in cell viability and all concentrations exhibited at least 100% cell viability compared with the normal control. In the positive control group, TGF-β1, a well-established inducer of EMT in vitro, the epithelial marker E-cadherin expression was significantly suppressed while the mesenchymal marker N-cadherin was significantly up-regulated. Conversely, TRAIL-treated BEAS-2B cells showed no significant changes in E-cadherin and N-cadherin expression compared to the untreated cells. Discussion: Our findings demonstrated that soluble TRAIL (up to 50 ng/mL) is not cytotoxic and not able to induce EMT in human bronchial epithelial cells. This could be due to the expression of TRAIL receptors on human bronchial epithelial cells that may regulate the effects of soluble TRAIL. Although further investigations may be required, this preliminary data suggest that TRAIL does not contribute to airway remodelling via its effects on EMT, rather TRAIL may be involved in other mechanisms that mediate airway remodelling. Conclusion: Soluble TRAIL does not promote the expression of key EMT markers, E-cadherin and N-cadherin in human bronchial epithelial cells in vitro.
| Item Type: | Project Paper |
|---|---|
| Faculty: | Faculty of Medicine and Health Science |
| Depositing User: | Ms. Nor Safa'aton Saidin |
| Date Deposited: | 22 Aug 2023 04:38 |
| Last Modified: | 22 Aug 2023 04:38 |
| URI: | http://psaspb.upm.edu.my/id/eprint/1348 |
Actions (login required)
 |
View Item |