The Regulation of TNF-Related Apoptosis Inducing Ligand (TRAIL) Expression in TGFB-Induced Bronchial Epithelial Mesenchymal Transition (EMT)

Che Ani, Noor Salsabila (2022) The Regulation of TNF-Related Apoptosis Inducing Ligand (TRAIL) Expression in TGFB-Induced Bronchial Epithelial Mesenchymal Transition (EMT). [Project Paper] (Submitted)

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Abstract

Asthma is an airway disease characterized by reversible airflow limitation and airway hyperresponsiveness, meanwhile chronic obstructive pulmonary disease (COPD) is characterized by its persistent airflow obstruction. Besides airway inflammation, structural changes in the airways, known as airway remodelling, also contributes to these asthmatic and COPD features. One of the prominent structural changes in airway remodelling is the alteration that occurs in the airway epithelium. It has been proposed that a biological process known as epithelial-mesenchymal transition (EMT) can contribute to airway remodelling. Increasing evidence suggests an association between airway remodelling and a molecule called tumor necrosis factor–related apoptosis inducing ligand (TRAIL). Although high levels of TRAIL have been reported in bronchial biopsy and bronchoalveolarlavage fluid from asthmatic patients, the biological role of TRAIL in the airway epithelium and its association with EMT still needs further understanding. Objective: This study aims to determine the association between EMT induction and TRAIL protein expression in human bronchial epithelial cells following acute and chronic treatment of TGFβ1. Methodology: Normal human bronchial epithelial cells (BEAS2B) cells were treated with TGFβ1 for 48 hours to induce acute induction of EMT, meanwhile for chronic induction of EMT, the BEAS2B cells were treated for 2 days, 4 days and 6 days. Western Blot was run to determine the expression of TRAIL and EMT markers (E-cadherin, N-cadherin and Vimentin) following acute and chronic induction of EMT by TGFβ1. Results: E-cadherin expression reduced while N-cadherin and Vimentin expression as well as TRAIL expression increased in human bronchial epithelial cells following acute and chronic induction of EMT by TGFβ1. Discussion: EMT induction by TGFβ1 in bronchial epithelial cells is successful and consistent with previous studies in which TRAIL is upregulated in human bronchial epithelial cells, that suggests epithelial cells is a source of TRAIL that contributes to the elevated TRAIL levels that has been reported in asthmatic and COPD patients. Conclusion: TRAIL expression has a positive correlation with TGFβ1-induced bronchial epithelial EMT.

Item Type:	Project Paper
Faculty:	Faculty of Medicine and Health Science
Depositing User:	Ms. Nor Safa'aton Saidin
Date Deposited:	22 Aug 2023 04:40
Last Modified:	22 Aug 2023 04:40
URI:	http://psaspb.upm.edu.my/id/eprint/1377

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