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    Normal human bronchial epithelial cells were studied to characterize epithelial-mesenchymal transition induced by cigarette smoke, a key driver of chronic obstructive pulmonary disease. Experiments showed that inducing EMT in differentiated NHBE cells decreased levels of E-cadherin, an adhesion protein, and also decreased ciliary beat frequency and ciliary abundance, demonstrating cellular changes linked to COPD through EMT. The research aims to better understand the role of EMT in the pathogenesis of COPD, which is a major cause of mortality worldwide.

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    Normal human bronchial epithelial cells were studied to characterize epithelial-mesenchymal transition induced by cigarette smoke, a key driver of chronic obstructive pulmonary disease. Experiments showed that inducing EMT in differentiated NHBE cells decreased levels of E-cadherin, an adhesion protein, and also decreased ciliary beat frequency and ciliary abundance, demonstrating cellular changes linked to COPD through EMT. The research aims to better understand the role of EMT in the pathogenesis of COPD, which is a major cause of mortality worldwide.

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    10 views1 page

    Agarwal Vanshika Abstract

    Uploaded by

    api-378886776
    Normal human bronchial epithelial cells were studied to characterize epithelial-mesenchymal transition induced by cigarette smoke, a key driver of chronic obstructive pulmonary disease. Experiments showed that inducing EMT in differentiated NHBE cells decreased levels of E-cadherin, an adhesion protein, and also decreased ciliary beat frequency and ciliary abundance, demonstrating cellular changes linked to COPD through EMT. The research aims to better understand the role of EMT in the pathogenesis of COPD, which is a major cause of mortality worldwide.

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    Characterizing Epithelial-Mesenchymal Transition in

    Normal Human Bronchial Epithelial cells

    Vanshika Agarwal

    Dr. Venkataramana Sidhaye

    Johns Hopkins Bloomberg School of Public Health

    Abstract:

    Chronic Obstructive Pulmonary Disease (COPD) is a major cause of mortality and soon to

    become the third leading cause of death in the world. COPD is characterized by chronic airflow

    limitation and continues to be largely irreversible. Cigarette smoke (CS) is one of the crucial

    factors that drives COPD. CS damages the epithelial barrier shown by increased monolayer

    permeability. It also tends to change the protein concentrations, especially in regard to adhesion

    proteins. Recently, similar changes in Epithelial Mesenchymal Transition (EMT) induced cells

    have related COPD to EMT. Our research characterizes how inducing EMT in differentiated

    NHBE cells decrease E-cadherin, decrease ciliary beat frequency (CBF), and ciliary abundance.

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