Methods: Human epithelial cells (A549 and BEAS-2B lines, primary) were cultured prior to stimulation using PAR2 agonists (SLIGKV, trypsin) and autophagy quantified using a fluorescent marker of autophagosomes (CYTO-ID detection kit). Western blotting to analyse expression of ATGs (autophagy related genes) was used to confirm findings. PAR2 cellular expression was assessed by immunofluorescence.
PAR2 expression was demonstrated in human airway epithelial cells. Autophagic vesicles were successfully detected, and fluorescence levels detected modulated by appropriate autophagy controls. Stimulation of PAR2 activity, assessed alone and in combination with inflammatory stimuli, also caused modulation of the level of autophagic activity within airway epithelial cultures.
Our data indicate PAR2 as a potential regulator of autophagy in lung airway epithelia, suggesting a possible novel role in conditions such as COPD that feature premature lung ageing.
|Publication status||Published - 5 Sep 2018|
|Event||British Association for Lung Research Summer Meeting 2018: Inflammation in the Ageing Lung - University of Birmingham, Birmingham , United Kingdom|
Duration: 5 Sep 2018 → 7 Sep 2018
|Conference||British Association for Lung Research Summer Meeting 2018|
|Period||5/09/18 → 7/09/18|
- Key Words - Ageing, Autophagy, PAR2, COPD, ATGs, Pulmonary, Epithelial
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John Lockhart, Gary Litherland, Anne Crilly, Carl Goodyear, Andrew MacKenzie, Iain McLellan, Andisheh Bakhshi, Lynette Dunning, Robin Freeburn, William MacKay, Craig Williams, Kirsty McCallum, Mariarca Bailo, Kimberly Black, Bryn Short, Mark Thomas & Fawziye Tarhini
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