The effect of TGFB-1-induced epithelial-mesenchymal transition on TRAIL expression in human bronchial epithelial cells

Pan, Swee Qi (2021) The effect of TGFB-1-induced epithelial-mesenchymal transition on TRAIL expression in human bronchial epithelial cells. [Project Paper] (Submitted)

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Abstract

Airway diseases including asthma and chronic obstructive pulmonary disease (COPD) are among the leading causes of death worldwide. Airway diseases are commonly characterised by chronic inflammation and airway remodelling which contribute to airflow limitation. Available treatments for airway diseases mainly act by suppressing airway inflammation, while strategies that target airway remodelling remain lacking. Epithelial-mesenchymal transition (EMT) is one of the pathophysiological features of airway remodelling whereby the epithelial cells lining the airway undergo transformation into mesenchymal cells, progressively losing epithelial markers such as E-cadherin while gaining mesenchymal markers such as N-cadherin. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a protein that has been implicated in airway diseases. Increasing evidence suggests that TRAIL deficiency is associated with reduced airway inflammation and remodelling in mouse models. However, the link between TRAIL and bronchial EMT has not yet been specifically addressed. Objective: This study aims to determine the association between TRAIL and features of EMT using an established cellular model of bronchial EMT, where TGFB1 is used as an EMT inducer. Hypothesis: It is hypothesized that TRAIL expression in human bronchial epithelial cells is upregulated in response to TGFB-1 and that this modulation is correlated with the changes in cell morphology and EMT markers expression associated with EMT. Methodology: Normal human bronchial epithelial (NHBE) cells will be treated with TGFB-1 for 48 hours to induce EMT. Morphological changes will be assessed and the cell radius ratio will be determined. TRAIL, E-cadherin and N-cadherin expression will be assessed by western blotting. Result: TGFB-1-treated NHBE cells displayed elongated shape with increased cell radius ratio, reduced E-cadherin expression and increased N-cadherin expression. Collectively, this suggests the activation of EMT that resulted the change in morphology of NHBE. Interestingly, TRAIL expression is found to be downregulated upon activation of EMT. Conclusion: TGFB-1-induced EMT is negatively correlated with the endogenous TRAIL expression. The hypothesis is rejected.

Item Type:	Project Paper
Faculty:	Faculty of Medicine and Health Science
Depositing User:	Ms. Nor Safa'aton Saidin
Date Deposited:	22 Aug 2023 07:49
Last Modified:	22 Aug 2023 07:49
URI:	http://psaspb.upm.edu.my/id/eprint/1125

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