Dr Andrew Reid

Dr Andrew Reid

Postdoctoral Researcher

School of Medicine and Public Health

Telescopes to Microscopes: an ingrained love for science

Dr Andrew Reid may have taken the long road to medical research, but it’s not one he regrets.

Dr Andrew Reid

“When I was still in high school my real passion was astronomy – my Dad had bought me a telescope and I got really into it."

“So when I started out at university, I was doing a double major in maths and physics.”

Hailing from the Central Coast, Andrew’s regular commute to Sydney for his studies was a gruelling one.

“Once I got to the third year it all got to be too much – I ended up deferring and I worked in retail for a while. Then one evening I was talking to my manager – who had always wanted to be a police officer – and we made a deal. He would join the police force and I would go back to university.”

Andrew transferred his credits to UON and was able to complete his science degree, but with a major in biology.

“It turns out biology and chemistry were my calling! I ended up getting First Class Honours and the University Medal.”

On top of those accolades, Andrew was also awarded the Faculty of Science Medal for best thesis and the Barry Boettcher Award for leading grade point average.

For his Honours and PhD projects, Andrew worked in UON’s Reproductive Science group, under the supervision of Dr Shaun Roman and Professor Brett Nixon, respectively.

Andrew’s PhD research focussed on the role of the dynamin protein in sperm maturation and fertilisation. For his work, he was awarded the New Investigator Award from the Australian Society of Reproductive Biology in 2011.

Focus on epithelium

The epithelial cell layer, or ‘epithelium’, occurs throughout the body wherever surfaces come into contact with the outside environment and also on the insides of vessels, tracts and tubules.

The architecture of epithelial cells is highly regulated, and the intracellular junctions are particularly important for maintaining function. These junctions are made up of protein complexes which allow cells to communicate, share nutrients and maintain physical contact with each other.

“The final chapter of my PhD thesis was actually on the epithelium of the epididymis – a duct within the male reproductive system."

“One of the good things about learning about those cells is they stay pretty similar throughout all the different areas of the body.”

Indeed, when Professor Darryl Knight was looking for help in his lab with an asthma research project with the PRC for Healthy Lungs, it turns out Andrew had experience in all the right areas.

“I’ve also got a lot of experience with fluorescence and electron microscopy.”

The disappearing mucus

Previous research by some of Darryl’s international collaborators had highlighted the significance of the Beta-catenin signalling pathway in airway disease, in particular in the epithelial cells lining the airways.

The amount of Beta-catenin protein in the intracellular junctions was different in asthmatic compared to non-asthmatic individuals.

Upon looking closer at this phenomenon, Darryl and Andrew noticed a strange effect of Beta-catenin blocking chemicals.

“Mucus production was decreasing – but it wasn’t via the normal mucus-stimulating cellular pathways. It instead appeared to be happening via the Notch Signalling pathway."

The Notch protein has been well described for its role in tissue development, but this direct involvement in mucus regulation was a novel observation.

Using a specialised cell culture technique, known as air liquid interface culture, researchers within the PRC for Healthy Lungs are able to grow human donor airway epithelial cells in the lab.

The cells differentiate into specific cell types and assume an architecture all but identical to that of the human respiratory epithelial layer.

“Every few days I’ve got to come in and wash off the mucus from the surface of my asthmatic cells and it’s all gluggy and horrible."

“But then when I inhibit Notch, you don’t get that mucus. The cells are all there and they’re happy, they’re still alive - they’re just not spitting out mucus.”

Looking ahead

As well as Notch appearing to regulate mucus production itself, it can also modify the characteristics of the mucus, making it less sticky.

This mucosal stickiness is a problem not just in asthmatics, but also for patients with chronic bronchitis and COPD (Chronic Obstructive Pulmonary Disease).

“We’re hoping to identify which interactions in the Notch signalling pathway are causing these changes in mucus production."

“Then we could design new pharmaceuticals targeting these proteins and increase the quality of life for these patients.”

It’s an exciting field, and one that Andrew’s looking forward to continuing to explore.

Telescopes to Microscopes: an ingrained love for science

Dr Andrew Reid has a hand in increasing the life of asthma patients.

Read more

Career Summary

Biography

Research overview

Dr Andrew Reid completed his Bachelor of Science (Hons I) degree in 2009 with a perfect grade point average and earning both the faculty and university medals. He was offered a prestigious Australian Postgraduate Award scholarship as well as the Deputy Vice Chancellor’s award to complete his PhD. Andrew's PhD on the role of dynamin in mouse spermatozoa and the epididymal epithelium earned him 3 high ranking publications during his PhD tenure. In addition to numerous scientific and artistic prizes throughout his tenure, Dr Reid was nominated for the PhD medal on the back of his exemplary studies.

In 2014, Andrew began his employment under world-renowned epithelial cell biologist Professor Darryl Knight at the Hunter Medical Research Institute. Here, Andrew's experience in a wide range of microscopy (including immunofluorescent, phase contrast and electron microscopy) and pharmacological inhibition techniques were adopted as no standard procedure. Dr Reid has published under Professor Knight on the roles of the signalling molecule beta-catenin during epithelial to mesenchymal transition, the contributions of genetic and epigenetic dysregulations in asthma and has recently published in Pharmacology and Therapeutics on the "Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches".

Currently, Andrew's investigations centre on the imbalance of certain developmental signalling pathways and how this contributes to increased mucus production and accumulation in the airway epithelium of asthmatics. As of January 2018, Dr. Reid has taken command of Conjoint Professor Chris Grainge’s most recently awarded NHMRC grant to investigate the role of mechanical forces at the dysregulated asthmatic airway epithelium.

Collaborations

Dr Reid has encouraged a number of local as well as international collaborations throughout his PhD and early post-doctoral career. Collaborations with UoN's own Professor Adam McCluskey (Chemistry) and Professor Phil Robinson of the Children's Medical Research Institute through Andrew's then PhD supervisor Professor Brett Nixon enabled the publication of Andrew's first two scientific manuscripts. Currently, collaborations with the James Hogg Research Institute (Canada) and Cornell University (New York) have provided Andrew with rare tissue samples and cells required for his epithelial mucus research.


Qualifications

  • Doctor of Philosophy, University of Newcastle

Keywords

  • Air-liquid Interface culture
  • Airway epithelium
  • Asthma
  • COPD
  • ELISA
  • Immunocytochemistry
  • Immunohistochemistry
  • Molecular biology
  • Mucus
  • Nanostring
  • Notch signalling
  • PCR
  • Western blotting
  • qPCR

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 50
060199 Biochemistry and Cell Biology not elsewhere classified 50

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Researcher University of Newcastle
School of Medicine and Public Health
Australia
Postdoctoral Researcher Priority Research Centre (PRC) for Healthy Lungs | The University of Newcastle
School of Medicine and Public Health
Australia
Postdoctoral Researcher University of Newcastle
School of Medicine and Public Health
Australia

Professional appointment

Dates Title Organisation / Department
31/1/2014 - 31/12/2017 Posdoctoral Researcher

During this time I performed experiments using primary bronchial epithelial cells grown at the air-liquid interface from asthmatic and non-asthmatic donors. I also Investigated the Notch and beta-catenin signalling pathways within asthmatic and non-asthmatic airways.  I performed pharmacological inhibition of these pathways and analysed the effects on airway morphology. I also developed a number of immunofluorescence and protein quantification techniques used in our laboratory today.

The University of Newcastle - School of Biomedical Sciences and Pharmacy
Respiratory
Australia

Awards

Award

Year Award
2010 University Medal
The University of Newcastle
2010 Faculty Medal
Faculty of Science and Information Technology,The University of Newcastle

Prize

Year Award
2017 Conference Travel Award
The Thoracic Society of Australia & New Zealand
2017 Cell/Biology/Immunology SIG award
The Thoracic Society of Australia and New Zealand
2016 Early Career Award
Priority Research Centre (PRC) for Healthy Lungs | The University of Newcastle
2013 Beautiful Science award
The University of Newcastle, School of Biomedical Sciences and Pharmacy
2012 Society for Reproductive Biology travel award
Australian Society for Reproductive Biology
2011 New Investigator Award
Australian Society of Reproductive Biology
2011 Society for Reproductive Biology travel award
Australian Society for Reproductive Biology
2010 Barry Boettcher Award
Faculty of Science and Information Technology,The University of Newcastle
2010 Australian Postgraduate Award
The University of Newcastle
2010 Deputy Vice Chancellor Research and Innovation Scholarship
The University of Newcastle

Teaching

Code Course Role Duration
BIOL3090 Molecular Biology
Faculty of Science and Information Technology, The University of Newcastle | Australia
Assessed and marked presentations given by students as per tutorial demonstrator role.
Head Tutorial Demonstrator 1/7/2010 - 30/6/2011
BIOL2001 Molecular Laboratory Skills for Biological Sciences
Faculty of Science and Information Technology, The University of Newcastle | Australia
Laboratory Demonstrator
Laboratory Demonstrator 2/3/2009 - 30/6/2009
BIOL2001 Molecular Laboratory Skills for Biological Sciences
Faculty of Science and Information Technology, The University of Newcastle | Australia
Head Laboratory Demonstrator
Laboratory Demonstrator 1/3/2010 - 30/6/2010
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Chapter (1 outputs)

Year Citation Altmetrics Link
2019 Reid AT, Sutanto EN, Chander-Veerati P, Looi K, Li NF, Iosifidis T, et al., 'Ground zero-the airway epithelium', Rhinovirus Infections: Rethinking the Impact on Human Health and Disease, Academic Press, Cambridge, MS 61-98 (2019) [B1]
DOI 10.1016/B978-0-12-816417-4.00003-2
Co-authors Punnam Veerati

Journal article (17 outputs)

Year Citation Altmetrics Link
2020 Baines KJ, Fricker M, McDonald VM, Simpson JL, Wood LG, Wark PAB, et al., 'Sputum transcriptomics implicates increased p38 signalling activity in severe asthma', Respirology, 25 709-718 (2020) [C1]

© 2019 Asian Pacific Society of Respirology Background and objective: Severe asthma is responsible for a disproportionate burden of illness and healthcare costs spent on asthma. T... [more]

© 2019 Asian Pacific Society of Respirology Background and objective: Severe asthma is responsible for a disproportionate burden of illness and healthcare costs spent on asthma. This study analyses sputum transcriptomics to investigate the mechanisms and novel treatment targets of severe asthma. Methods: Induced sputum samples were collected in a cross-sectional study from participants with severe asthma (n = 12, defined as per GINA criteria), non-severe uncontrolled (n = 21) and controlled asthma (n = 21) and healthy controls (n = 15). Sputum RNA was extracted and transcriptomic profiles were generated (Illumina HumanRef-8 V2) and analysed (GeneSpring). Sputum protein lysates were analysed for p38 activation in a validation study (n = 24 asthma, n = 8 healthy) by western blotting. Results: There were 2166 genes differentially expressed between the four groups. In severe asthma, the expression of 1875, 1308 and 563 genes was altered compared to healthy controls, controlled and uncontrolled asthma, respectively. Of the 1875 genes significantly different to healthy controls, 123 were >2-fold change from which four networks were identified. Thirty genes (>2-fold change) were significantly different in severe asthma compared to both controlled asthma and healthy controls. There was enrichment of genes in the p38 signalling pathway that were associated with severe asthma. Phosphorylation of p38 was increased in a subset of severe asthma samples, correlating with neutrophilic airway inflammation. Conclusion: Severe asthma is associated with substantial differences in sputum gene expression that underlie unique cellular mechanisms. The p38 signalling pathway may be important in the pathogenesis of severe asthma, and future investigations into p38 inhibition are warranted as a ¿non-Th2¿ therapeutic option.

DOI 10.1111/resp.13749
Citations Scopus - 2Web of Science - 1
Co-authors Peter Gibson, Peter Wark, Katherine Baines, Jodie Simpson, Lisa Wood, Vanessa Mcdonald, Michael Fricker
2020 Schuliga M, Read J, Blokland KEC, Waters DW, Burgess J, Prele C, et al., 'Self DNA perpetuates IPF lung fibroblast senescence in a cGAS-dependent manner', CLINICAL SCIENCE, 134 889-905 (2020) [C1]
DOI 10.1042/CS20191160
Citations Scopus - 4Web of Science - 4
Co-authors Darryl Knight, Christopher Grainge, Michael Schuliga
2020 Veerati PC, Mitchel JA, Reid AT, Knight DA, Bartlett NW, Park JA, Grainge CL, 'Airway mechanical compression: Its role in asthma pathogenesis and progression', European Respiratory Review, 29 1-13 (2020) [C1]
DOI 10.1183/16000617.0123-2019
Citations Scopus - 1
Co-authors Christopher Grainge, Nathan Bartlett, Punnam Veerati, Darryl Knight
2020 Kicic A, de Jong E, Ling K-M, Nichol K, Anderson D, Wark PAB, et al., 'Assessing the unified airway hypothesis in children via transcriptional profiling of the airway epithelium', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 145 1562-1573 (2020) [C1]
DOI 10.1016/j.jaci.2020.02.018
Citations Scopus - 1Web of Science - 1
Co-authors Peter Wark, Darryl Knight, Punnam Veerati
2020 Reid AT, Nichol KS, Veerati PC, Moheimani F, Kicic A, Stick SM, et al., 'Blocking notch3 signaling abolishes MUC5AC production in airway epithelial cells from individuals with asthma', American Journal of Respiratory Cell and Molecular Biology, 62 513-523 (2020) [C1]

Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more dif... [more]

Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more difficult to clear and results in airway mucus plugging. Notch1, Notch2, or Notch3, or a combination of these has been shown to influence the differentiation of airway epithelial cells. How the expression of specific Notch isoforms differs in fully differentiated adult asthmatic epithelium and whether Notch influences mucin production after differentiation is currently unknown. We aimed to quantify different Notch isoforms in the airway epithelium of individuals with severe asthma and to examine the impact of Notch signaling on mucin MUC5AC. Human lung sections and primary bronchial epithelial cells from individuals with and without asthma were used in this study. Primary bronchial epithelial cells were differentiated at the air-liquid interface for 28 days. Notch isoform expression was analyzed by Taqman quantitative PCR. Immunohistochemistry was used to localize and quantify Notch isoforms in human airway sections. Notch signaling was inhibited in vitro using dibenzazepine or Notch3-specific siRNA, followed by analysis of MUC5AC. NOTCH3 was highly expressed in asthmatic airway epithelium compared with nonasthmatic epithelium. Dibenzazepine significantly reduced MUC5AC production in air-liquid interface cultures of primary bronchial epithelial cells concomitantly with suppression of NOTCH3 intracellular domain protein. Specific knockdown using NOTCH3 siRNA recapitulated the dibenzazepine-induced reduction in MUC5AC. We demonstrate that NOTCH3 is a regulator of MUC5AC production. Increased NOTCH3 signaling in the asthmatic airway epithelium may therefore be an underlying driver of excess MUC5AC production.

DOI 10.1165/rcmb.2019-0069OC
Citations Scopus - 3Web of Science - 3
Co-authors Punnam Veerati, Darryl Knight, Fatemeh Moheimani, Nathan Bartlett, Peter Wark, Christopher Grainge, Philip Hansbro
2020 Veerati PC, Troy NM, Reid AT, Li NF, Nichol KS, Kaur P, et al., 'Airway Epithelial Cell Immunity Is Delayed During Rhinovirus Infection in Asthma and COPD', Frontiers in Immunology, 11 (2020)

© Copyright © 2020 Veerati, Troy, Reid, Li, Nichol, Kaur, Maltby, Wark, Knight, Bosco, Grainge and Bartlett. Respiratory viral infections, particularly those caused by rhinovirus,... [more]

© Copyright © 2020 Veerati, Troy, Reid, Li, Nichol, Kaur, Maltby, Wark, Knight, Bosco, Grainge and Bartlett. Respiratory viral infections, particularly those caused by rhinovirus, exacerbate chronic respiratory inflammatory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible of initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response (including type I and type III interferon) in asthma is less effective or deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. However, deficient rhinovirus-induced epithelial interferon production in asthma has not always been observed. We hypothesized that disparate in vitro airway epithelial infection models using high multiplicity of infection (MOI) and lacking genome-wide, time course analyses have obscured the role of epithelial innate anti-viral immunity in asthma and COPD. To address this, we developed a low MOI rhinovirus model of differentiated primary epithelial cells obtained from healthy, asthma and COPD donors. Using genome-wide gene expression following infection, we demonstrated that gene expression patterns are similar across patient groups, but that the kinetics of induction are delayed in cells obtained from asthma and COPD donors. Rhinovirus-induced innate immune responses were defined by interferons (type-I, II, and III), interferon response factors (IRF1, IRF3, and IRF7), TLR signaling and NF-¿B and STAT1 activation. Induced gene expression was evident at 24 h and peaked at 48 h post-infection in cells from healthy subjects. In contrast, in cells from donors with asthma or COPD induction was maximal at or beyond 72¿96 h post-infection. Thus, we propose that propensity for viral exacerbations of asthma and COPD relate to delayed (rather than deficient) expression of epithelial cell innate anti-viral immune genes which in turns leads to a delayed and ultimately more inflammatory host immune response.

DOI 10.3389/fimmu.2020.00974
Co-authors Christopher Grainge, Darryl Knight, Peter Wark, Nathan Bartlett, Punnam Veerati, Steven Maltby
2019 Singanayagam A, Loo SL, Calderazzo M, Finney LJ, Torralbo MBT, Bakhsoliani E, et al., 'Antiviral immunity is impaired in COPD patients with frequent exacerbations', American Journal of Physiology - Lung Cellular and Molecular Physiology, 317 L893-L903 (2019) [C1]

© the American Physiological Society. Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. Th... [more]

© the American Physiological Society. Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine the innate immune mechanisms that underlie susceptibility to frequent exacerbations in COPD. We measured sputum expression of immune mediators and bacterial loads in samples from patients with COPD at stable state and during virusassociated exacerbations. In vitro immune responses to rhinovirus infection in differentiated primary bronchial epithelial cells (BECs) sampled from patients with COPD were additionally evaluated. Patients were stratified as frequent exacerbators (=2 exacerbations in the preceding year) or infrequent exacerbators (<2 exacerbations in the preceding year) with comparisons made between these groups. Frequent exacerbators had reduced sputum cell mRNA expression of the antiviral immune mediators type I and III interferons and reduced interferon-stimulated gene (ISG) expression when clinically stable and during virus-associated exacerbation. A role for epithelial cellintrinsic innate immune dysregulation was identified: induction of interferons and ISGs during in vitro rhinovirus (RV) infection was also impaired in differentiated BECs from frequent exacerbators. Frequent exacerbators additionally had increased sputum bacterial loads at 2 wk following virus-associated exacerbation onset. These data implicate deficient airway innate immunity involving epithelial cells in the increased propensity to exacerbations observed in some patients with COPD. Therapeutic approaches to boost innate antimicrobial immunity in the lung could be a viable strategy for prevention and treatment of frequent exacerbations.

DOI 10.1152/ajplung.00253.2019
Citations Scopus - 9Web of Science - 8
Co-authors Jason Girkin, Punnam Veerati, Nathan Bartlett, Christopher Grainge, Peter Wark
2018 Reid AT, Veerati PC, Gosens R, Bartlett NW, Wark PA, Grainge CL, et al., 'Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches', Pharmacology and Therapeutics, 185 155-169 (2018) [C1]

© 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To... [more]

© 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.

DOI 10.1016/j.pharmthera.2017.12.009
Citations Scopus - 12Web of Science - 12
Co-authors Darryl Knight, Christopher Grainge, Punnam Veerati, Fatemeh Moheimani, Nathan Bartlett, Peter Wark, Philip Hansbro
2018 Schuliga M, Pechkovsky DV, Read J, Waters DW, Blokland KEC, Reid AT, et al., 'Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts', JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 22 5847-5861 (2018)
DOI 10.1111/jcmm.13855
Citations Scopus - 23Web of Science - 25
Co-authors Christopher Grainge, Darryl Knight, Michael Schuliga
2018 Singanayagam A, Glanville N, Girkin JL, Ching YM, Marcellini A, Porter JD, et al., 'Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations', NATURE COMMUNICATIONS, 9 (2018) [C1]
DOI 10.1038/s41467-018-04574-1
Citations Scopus - 44Web of Science - 41
Co-authors Darryl Knight, Christopher Grainge, Peter Wark, Nathan Bartlett, Jason Girkin, Punnam Veerati
2018 Moheimani F, Koops J, Williams T, Reid AT, Hansbro PM, Wark PA, Knight DA, 'Influenza A virus infection dysregulates the expression of microRNA-22 and its targets; CD147 and HDAC4, in epithelium of asthmatics', Respiratory Research, 19 (2018) [C1]
DOI 10.1186/s12931-018-0851-7
Citations Scopus - 12Web of Science - 13
Co-authors Peter Wark, Philip Hansbro, Fatemeh Moheimani, Darryl Knight
2017 Zhou W, De Iuliis GN, Turner AP, Reid AT, Anderson AL, McCluskey A, et al., 'Developmental expression of the dynamin family of mechanoenzymes in the mouse epididymis', BIOLOGY OF REPRODUCTION, 96 159-173 (2017) [C1]
DOI 10.1095/biolreprod.116.145433
Citations Scopus - 9Web of Science - 8
Co-authors Geoffry DeiuliIs, Eileen Mclaughlin, Brett Nixon, Adam Mccluskey
2016 Moheimani F, Hsu AC-Y, Reid AT, Williams T, Kicic A, Stick SM, et al., 'The genetic and epigenetic landscapes of the epithelium in asthma', RESPIRATORY RESEARCH, 17 (2016) [C1]
DOI 10.1186/s12931-016-0434-4
Citations Scopus - 32Web of Science - 32
Co-authors Alan Hsu, Philip Hansbro, Fatemeh Moheimani, Peter Wark, Darryl Knight
2015 Moheimani F, Roth HM, Cross J, Reid AT, Shaheen F, Warner SM, et al., 'Disruption of ß-catenin/CBP signaling inhibits human airway epithelial-mesenchymal transition and repair', International Journal of Biochemistry and Cell Biology, 68 59-69 (2015) [C1]

© 2015 Elsevier Ltd. The epithelium of asthmatics is characterized by reduced expression of E-cadherin and increased expression of the basal cell markers ck-5 and p63 that is indi... [more]

© 2015 Elsevier Ltd. The epithelium of asthmatics is characterized by reduced expression of E-cadherin and increased expression of the basal cell markers ck-5 and p63 that is indicative of a relatively undifferentiated repairing epithelium. This phenotype correlates with increased proliferation, compromised wound healing and an enhanced capacity to undergo epithelial-mesenchymal transition (EMT). The transcription factor ß-catenin plays a vital role in epithelial cell differentiation and regeneration, depending on the co-factor recruited. Transcriptional programs driven by the ß-catenin/CBP axis are critical for maintaining an undifferentiated and proliferative state, whereas the ß-catenin/p300 axis is associated with cell differentiation. We hypothesized that disrupting the ß-catenin/CBP signaling axis would promote epithelial differentiation and inhibit EMT. We treated monolayer cultures of human airway epithelial cells with TGFß1 in the presence or absence of the selective small molecule ICG-001 to inhibit ß-catenin/CBP signaling. We used western blots to assess expression of an EMT signature, CBP, p300, ß-catenin, fibronectin and ITGß1 and scratch wound assays to assess epithelial cell migration. Snai-1 and -2 expressions were determined using q-PCR. Exposure to TGFß1 induced EMT, characterized by reduced E-cadherin expression with increased expression of a-smooth muscle actin and EDA-fibronectin. Either co-treatment or therapeutic administration of ICG-001 completely inhibited TGFß1-induced EMT. ICG-001 also reduced the expression of ck-5 and -19 independent of TGFß1. Exposure to ICG-001 significantly inhibited epithelial cell proliferation and migration, coincident with a down regulation of ITGß1 and fibronectin expression. These data support our hypothesis that modulating the ß-catenin/CBP signaling axis plays a key role in epithelial plasticity and function.

DOI 10.1016/j.biocel.2015.08.014
Citations Scopus - 30Web of Science - 29
Co-authors Fatemeh Moheimani, Darryl Knight, Philip Hansbro
2015 Reid AT, Anderson AL, Roman SD, McLaughlin EA, McCluskey A, Robinson PJ, et al., 'Glycogen synthase kinase 3 regulates acrosomal exocytosis in mouse spermatozoa via dynamin phosphorylation', FASEB JOURNAL, 29 2872-2882 (2015) [C1]
DOI 10.1096/fj.14-265553
Citations Scopus - 13Web of Science - 12
Co-authors Eileen Mclaughlin, Brett Nixon, Shaun Roman, John Aitken, Adam Mccluskey
2012 Reid AT, Lord T, Stanger SJ, Roman SD, McCluskey A, Robinson PJ, et al., 'Dynamin regulates specific membrane fusion events necessary for acrosomal exocytosis in mouse spermatozoa', Journal of Biological Chemistry, 287 37659-37672 (2012) [C1]
Citations Scopus - 36Web of Science - 36
Co-authors Tessa Lord, John Aitken, Shaun Roman, Adam Mccluskey, Brett Nixon
2010 Reid AT, Redgrove KA, Aitken RJ, Nixon B, 'Cellular mechanisms regulating sperm-zona pellucida interaction', Asian Journal of Andrology, 13 88-96 (2010) [C1]
DOI 10.1038/aja.2010.74
Citations Scopus - 48Web of Science - 43
Co-authors John Aitken, Brett Nixon, Kate Redgrove
Show 14 more journal articles

Conference (14 outputs)

Year Citation Altmetrics Link
2019 Li N, Reid AT, Nichol KS, Grainge C, Wark PAB, Knight DA, Bartlett NW, 'Differentiating Bronchial Epithelial Cells from Patients with Asthma Display Prolonged Repair and Delayed Barrier Formation', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Dallas, TX (2019)
Co-authors Christopher Grainge, Peter Wark, Nathan Bartlett, Darryl Knight
2019 Kuchibhotla VNS, Read J, Heijink IH, Nawijn MC, Reid A, Knight DA, 'Late Breaking Abstract - Role of beta-catenin and Notch signalling in increased airway mucous cell differentiation in asthma', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.OA3602
Citations Web of Science - 1
2019 Veerati PC, Reid A, Nichol K, Wark P, Bartlett N, Knight D, Grainge C, 'Asthmatic airway epithelial cells subjected to apical mechanical stress exhibit suppressed interferon release following viral infection', EUROPEAN RESPIRATORY JOURNAL, Madrid, SPAIN (2019)
DOI 10.1183/13993003.congress-2019.PA3337
Co-authors Nathan Bartlett, Peter Wark, Christopher Grainge
2018 Reid AT, Nichol KS, Wei L, Moheimani F, Bartlett NW, Hansbro PM, et al., 'Inhibition of NOTCH3 Signaling Abolishes MUC5AC Production in Human Airway Epithelial Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Co-authors Peter Wark, Nathan Bartlett, Christopher Grainge, Fatemeh Moheimani, Philip Hansbro, Darryl Knight
2017 Reid A, Moheimani F, Nichol K, Bartlett N, Wark P, Grainge C, Knight D, 'ACUTE INHIBITION OF NOTCH SIGNALLING ABLATES MUC5AC PRODUCTION IN HUMAN AIRWAY EPITHELIAL CELLS FROM ASTHMATIC, NON-ASTHMATIC AND COPD DONORS.', RESPIROLOGY (2017)
Citations Web of Science - 1
Co-authors Darryl Knight, Peter Wark, Christopher Grainge, Nathan Bartlett, Fatemeh Moheimani
2017 Moheimani F, Williams T, Koops J, Reid AT, Hansbro PM, Wark PAB, Knight D, 'Micrornas As Potential Epigenetic Targets To Restore The Airway Epithelium Integrity In Asthmatics', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Peter Wark, Darryl Knight, Philip Hansbro, Fatemeh Moheimani
2017 Reid AT, Moheimani F, Nichol K, Bartlett N, Wark PAB, Grainge C, et al., 'Short-Term Inhibition Of Notch Signalling Ablates Muc5ac Production In Human Airway Epithelial Cells From Asthmatic, Non-Asthmatic And COPD Donors', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Fatemeh Moheimani, Darryl Knight, Nathan Bartlett, Christopher Grainge, Philip Hansbro, Peter Wark
2016 Moheimani F, Koops J, Williams T, Reid A, Wark P, Knight D, 'MICRORNAS EXPRESSION ABNORMALITIES IN ASTHMATIC EPITHELIAL CELLS', Respirology, Perth, WA (2016)
Co-authors Darryl Knight, Fatemeh Moheimani, Peter Wark
2016 Moheimani F, Koops J, Williams T, Reid AT, Hansbro PM, Wark PA, Knight DA, 'ABNORMAL MICRORNAS EXPRESSION IN EPITHELIAL CELLS OF SEVERE ASTHMATICS', RESPIROLOGY (2016)
Co-authors Peter Wark, Darryl Knight, Philip Hansbro, Fatemeh Moheimani
2015 Moheimani F, Roth H, Cross J, Reid A, Shaheen F, Warner S, et al., 'SUPPRESSION OF beta-CATENIN/CBP SIGNALING INHIBITS EPITHELIAL-MESENCHYMAL TRANSITION AND MIGRATION OF HUMAN AIRWAY EPITHELIUM', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Philip Hansbro, Fatemeh Moheimani, Darryl Knight
2010 Reid AT, McEwan K, Campbell DM, Jans DA, Roman SD, 'Consistent nucleosome retention during chromatin packaging in human spermatozoa', OzBio 2010: The Molecules of Life - from Discovery to Biotechnology. Poster Abstracts, Melbourne, Vic (2010) [E3]
Co-authors Shaun Roman
2010 Reid AT, Roman SD, Aitken RJ, Nixon B, 'Investigation of the role of dynamin in sperm surface remodelling', OzBio 2010: The Molecules of Life - from Discovery to Biotechnology. Poster Abstracts, Melbourne, Vic (2010) [E3]
Co-authors Shaun Roman, John Aitken
2010 Roman SD, Reid AT, McEwan K, Campbell DM, Jans DA, 'Nucleosome Retention During Chromatin Packaging in Spermatozoa', Reproduction, Fertility and Development, Sydney (2010) [E3]
Co-authors Shaun Roman
2010 Reid AT, Roman SD, Aitken RJ, Nixon B, 'Characterisation of the GTPASE dynamin throughout murine sperm maturation', Reproduction, Fertility and Development, Sydney, NSW (2010) [E3]
Co-authors Shaun Roman, John Aitken
Show 11 more conferences
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Grants and Funding

Summary

Number of grants 7
Total funding $149,687

Click on a grant title below to expand the full details for that specific grant.


20191 grants / $32,225

The role of apical mechanical shear stress on epithelial cell function in asthma$32,225

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Andrew Reid, Doctor Punnam Chander Veerati, Conjoint Associate Professor Christopher Grainge, Conjoint Associate Professor Christopher Grainge
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2020
GNo G1900261
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

20182 grants / $41,057

Establishing a comprehensive in vitro model of bronchiectasis$23,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Associate Professor Christopher Grainge, Doctor Andrew Reid, Conjoint Professor Peter Wark, Doctor Katie Baines, Doctor Benjamin Vaughan, Doctor Punnam Chander Veerati
Scheme Research Grant
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo G1901576
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

The role of apical mechanical shear stress on epithelial cell function in asthma$17,307

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Andrew Reid, Doctor Punnam Chander Veerati, Conjoint Associate Professor Christopher Grainge
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800434
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

20173 grants / $58,420

Zeiss ApoTome.2 Optical Slider assembly$31,458

Funding body: The University of Newcastle

Funding body The University of Newcastle
Project Team

Foster, P.S., Knight, D.A., Kim, R.Y., Horvat J.C., Bartlett, N.W., Yang, M., Donovan, C., Starkey, M.R., Reid, A.T., Tay, H.L., Kaiko, G., Collison, A.M.

Scheme UON 2017 Researcher Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding Internal
Category INTE
UON N

Hunter Medical Research Institute Equipment Grant$19,198

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Project Team

D.A. Knight, N.W. Bartlett, C.L. Grainge, M. Schuliga, M.T. Liang, A.T. Reid

Scheme HMRI Equipment Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding Internal
Category INTE
UON N

Development of a medium throughput assay for assessing compounds that modulate fibroblast function in COPD$7,764

Funding body: Metera Pharmaceuticals Inc

Funding body Metera Pharmaceuticals Inc
Project Team Professor Darryl Knight, Dr Michael Schuliga, Doctor Andrew Reid
Scheme Research Consultancy
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701512
Type Of Funding C3212 - International Not for profit
Category 3212
UON Y

20161 grants / $17,985

Upgrades for existing Zeiss Automated Fluorescent Microscope$17,985

Funding body: The University of Newcastle

Funding body The University of Newcastle
Project Team

Starkey, M.R., Donovan, C., Kim, R.Y., Reid, A.T., Tay, H.L.

Scheme UoN Researcher Equipment Grant 2016
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo
Type Of Funding Internal
Category INTE
UON N
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Research Supervision

Number of supervisions

Completed1
Current2

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2018 PhD The Role of Beta-catenin in the Development of the Asthmatic Epithelial Phenotype PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD The cross-talk between STAT proteins drives dysfunctional epithelial responses to viruses in asthma PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2019 PhD Role of Mechanical Forces in Asthma Pathogenesis PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Dr Andrew Reid

Position

Postdoctoral Researcher
Knight Group
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email andrew.reid@newcastle.edu.au
Phone (02) 4042 0108

Office

Room HMRI2109
Building Hunter Medical Research Institute
Location New Lambton Heights

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