Defective cell migration as a mechanism of dysregulated asthmatic airway repair

Thomas Iosifidis

doi:10.26182/5b5ffb0769565

Defective cell migration as a mechanism of dysregulated asthmatic airway repair

Thomas Iosifidis

UWA Medical School

Research output: Thesis › Doctoral Thesis

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Abstract

The airway epithelium of children with asthma is characterised by abnormal wound repair that may contribute to disease pathobiology. This thesis reports defective cell migration compromises asthmatic airway epithelial repair. One of the contributing mechanisms was reduced integrin a5111 expression that resulted in dysregulated migration and defective repair in cultures of asthmatic children. Furthermore, Notch signalling was shown to be dysregulated in the asthmatic airway epithelium and partially regulate integrin a5 and repair. Finally, RNA-Sequencing identified a multitude of pathways to be altered in asthma with therapeutic potential to direct future research into novel therapeutics targeting asthmatic airway epithelial restitution.

Original language	English
Qualification	Doctor of Philosophy
Awarding Institution	The University of Western Australia
Supervisors/Advisors	Kicic, Anthony, Supervisor Stick, Stephen, Supervisor Sutanto, Erika, Supervisor Devadason, Sunalene, Supervisor
Thesis sponsors	Australian Government Research Training Program
Award date	11 Jul 2018
DOIs	https://doi.org/10.26182/5b5ffb0769565
Publication status	Unpublished - 2017

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THESIS - DOCTOR OF PHILOSOPHY - IOSIFIDIS Thomas - 2018
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Cite this

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title = "Defective cell migration as a mechanism of dysregulated asthmatic airway repair",

abstract = "The airway epithelium of children with asthma is characterised by abnormal wound repair that may contribute to disease pathobiology. This thesis reports defective cell migration compromises asthmatic airway epithelial repair. One of the contributing mechanisms was reduced integrin a5111 expression that resulted in dysregulated migration and defective repair in cultures of asthmatic children. Furthermore, Notch signalling was shown to be dysregulated in the asthmatic airway epithelium and partially regulate integrin a5 and repair. Finally, RNA-Sequencing identified a multitude of pathways to be altered in asthma with therapeutic potential to direct future research into novel therapeutics targeting asthmatic airway epithelial restitution. ",

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AB - The airway epithelium of children with asthma is characterised by abnormal wound repair that may contribute to disease pathobiology. This thesis reports defective cell migration compromises asthmatic airway epithelial repair. One of the contributing mechanisms was reduced integrin a5111 expression that resulted in dysregulated migration and defective repair in cultures of asthmatic children. Furthermore, Notch signalling was shown to be dysregulated in the asthmatic airway epithelium and partially regulate integrin a5 and repair. Finally, RNA-Sequencing identified a multitude of pathways to be altered in asthma with therapeutic potential to direct future research into novel therapeutics targeting asthmatic airway epithelial restitution.

KW - cell biology

KW - asthma

KW - epithelium

KW - airway

KW - repair

KW - cell migration

KW - mechanisms

KW - paediatrics

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DO - 10.26182/5b5ffb0769565

M3 - Doctoral Thesis

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Defective cell migration as a mechanism of dysregulated asthmatic airway repair

Abstract

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