Dr Michael Schuliga

Dr Michael Schuliga

Post-Doctoral Fellow

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr. Schuliga is an honours graduate of the University of Melbourne, and has become a dedicated biomedical scientist. He is currently situated at the Hunter Medical Research Insitute (HMRI). However, the majority of his post-doc life has been in the Dept. of Pharmacology & Therapeutics (University of Melbourne, 2002-2016) where he implemented advanced molecular biology and proteomic procedures in respiratory disease and cancer research. For the first 7 years, his research effort was primarily invested in commercial translational studies examining the mechanisms of action of novel anti-fibrotics for Biotech. Since 2009, his primary research focus has shifted towards non-commercial funded research programs in lung cell-molecular pharmacology, being CI on NHMRC project grants. Dr Schuliga is well networked in the lung fibrosis research community, currently advancing IPF research in team with Prof Darryl Knight and clinical lead, A/Prof Chris Grainge (University of Newcastle, HMRI). His numerous first- or senior-author original research publications in the premier specialist journals, British J Pharmacol, Am J Respir Cell Mol Biol (+5) and Am J Physiol Lung Cell Mol Physiol, show his pioneering research in the field. Dr Schuliga’s increasing profile is also highlighted by his recent invited reviews on the subject in Current Opinion in Pharmacology, Pulmonary Pharmacology & Therapeutics, Mediators of Inflammation and Biomolecules. Dr Schuliga has been invited speaker at international meetings including the Young Investigator’s International Smooth Muscle Symposia (2007, 2013 & 2015) and the British Association of Lung Research (BALR) Respiratory Genetics Meeting (2014). Dr. Schuliga has also presented at the Groningen Research Institute of Asthma and COPD (Netherlands, 2013) and annual meetings of the European Respiratory Society (ERS) and American Thoracic Society (ATS). He also regularly presents, judges and chairs sessions at national conferences held by ASCEPT, AHMRC and TSANZ and is on the organizing committee for Airway Inflammation and Remodelling (AIR) meetings. Dr Schuliga has been a recipient of the ATS International Travel Trainee Scholar Award and the BALR Travel Award. Furthermore, he was recently awarded the best presentation for the Parenchymal Lung Diseases session at the TSANZ NSW/ACT ASM (2016), a John Hunter Hospital Charitable Trust Grant (2017) and a Lung Foundation Australia, Lizotte Family IPF Research Grant (2017).


Qualifications

  • Doctor of Philosophy, Deakin University
  • Bachelor of Science, University of Melbourne
  • Graduate Diploma in Education (Secondary), Monash University

Keywords

  • Idiopathic pulmonary fibrosis
  • Senescence
  • Urokinase plasminogen activator
  • fibroblasts
  • lung disease
  • pharmacology
  • tissue remodelling

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 100

Professional Experience

UON Appointment

Title Organisation / Department
Post-Doctoral Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Awards

Prize

Year Award
2016 1st prize of the ILD Session (Oral Communication) at the TSANZ NSW Branch ASM (2016)
The Thoracic Society of Australia & New Zealand
2014 Travel Award by the British Association of Lung Research (BALR) (2014)
British Lung Foundation

Research Award

Year Award
2017 Lung Foundation Australia, Lizotte Family IPF Research Award
Lung Foundation Australia
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Publications

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


Chapter (5 outputs)

Year Citation Altmetrics Link
2015 Schuliga M, 'Airway smooth muscle, matrix and proteases: Therapeutic implications', Muscle Cell and Tissue, InTech, Online (2015)
DOI 10.5772/59347
2011 Stewart AG, Soon L, Schuliga M, 'Fibroblasts', Inflammation and Allergy Drug Design 149-162 (2011)
DOI 10.1002/9781444346688.ch11
2010 Schuliga M, Braet F, Soon LL, Stewart AG, Chien H-Y, Ratinac KR, 'The benefits of microfluidics for imaging cell migration', Microscopy: Science, Technology, Applications and Education., Formatex Research Centre, Spain 1146-1154 (2010)
2003 Snow ET, Hu Y, Klein CB, McCluskey KL, Schuliga M, Sykora P, 'Regulation of redox and DNA repair genes by arsenic: low dose protection against oxidative stress?', , ELSEVIER SCIENCE BV 305-319 (2003)
DOI 10.1016/B978-044451441-7/50024-5
Citations Scopus - 9Web of Science - 3
2001 Snow ET, Schuliga M, Chouchane S, Hu Y, 'Sub-toxic arsenite induces a multi-component protective response against oxidative stress in human cells', , ELSEVIER SCIENCE BV 265-275 (2001)
Citations Web of Science - 1
Show 2 more chapters

Journal article (32 outputs)

Year Citation Altmetrics Link
2017 Murtha LA, Schuliga MJ, Mabotuwana NS, Hardy SA, Waters DW, Burgess JK, et al., 'The processes and mechanisms of cardiac and pulmonary fibrosis', Frontiers in Physiology, 8 (2017)

© 2017 Murtha, Schuliga, Mabotuwana, Hardy, Waters, Burgess, Knight and Boyle. Fibrosis is the formation of fibrous connective tissue in response to injury. It is characterized b... [more]

© 2017 Murtha, Schuliga, Mabotuwana, Hardy, Waters, Burgess, Knight and Boyle. Fibrosis is the formation of fibrous connective tissue in response to injury. It is characterized by the accumulation of extracellular matrix components, particularly collagen, at the site of injury. Fibrosis is an adaptive response that is a vital component of wound healing and tissue repair. However, its continued activation is highly detrimental and a common final pathway of numerous disease states including cardiovascular and respiratory disease. Worldwide, fibrotic diseases cause over 800,000 deaths per year, accounting for ~45% of total deaths. With an aging population, the incidence of fibrotic disease and subsequently the number of fibrosis-related deaths will rise further. Although, fibrosis is a well-recognized cause of morbidity and mortality in a range of disease states, there are currently no viable therapies to reverse the effects of chronic fibrosis. Numerous predisposing factors contribute to the development of fibrosis. Biological aging in particular, interferes with repair of damaged tissue, accelerating the transition to pathological remodeling, rather than a process of resolution and regeneration. When fibrosis progresses in an uncontrolled manner, it results in the irreversible stiffening of the affected tissue, which can lead to organ malfunction and death. Further investigation into the mechanisms of fibrosis is necessary to elucidate novel, much needed, therapeutic targets. Fibrosis of the heart and lung make up a significant proportion of fibrosis-related deaths. It has long been established that the heart and lung are functionally and geographically linked when it comes to health and disease, and thus exploring the processes and mechanisms that contribute to fibrosis of each organ, the focus of this review, may help to highlight potential avenues of therapeutic investigation.

DOI 10.3389/fphys.2017.00777
Co-authors Lucy Murtha, Darryl Knight, Andrew Boyle
2017 Schuliga M, Jaffar J, Harris T, Knight DA, Westall G, Stewart AG, 'The fibrogenic actions of lung fibroblast-derived urokinase: A potential drug target in IPF', Scientific Reports, 7 1-11 (2017) [C1]
DOI 10.1038/srep41770
Citations Scopus - 2Web of Science - 2
Co-authors Darryl Knight
2017 Schuliga M, Jaffar J, Berhan A, Langenbach S, Harris T, Waters D, et al., 'Annexin A2 contributes to lung injury and fibrosis by augmenting factor Xa fibrogenic activity', American Journal of Physiology - Lung Cellular and Molecular Physiology, 312 L772-L782 (2017) [C1]

© 2017 the American Physiological Society. In lung injury and disease, including idiopathic pulmonary fibrosis (IPF), extravascular factor X is converted into factor Xa (FXa), a ... [more]

© 2017 the American Physiological Society. In lung injury and disease, including idiopathic pulmonary fibrosis (IPF), extravascular factor X is converted into factor Xa (FXa), a coagulant protease with fibrogenic actions. Extracellular annexin A2 binds to FXa, augmenting activation of the protease-activated receptor-1 (PAR-1). In this study, the contribution of annexin A2 in lung injury and fibrosis was investigated. Annexin A2 immunoreactivity was observed in regions of fibrosis, including those ass ociated with fibroblasts in lung tissue of IPF patients. Furthermore, annexin A2 was detected in the conditioned media and an EGTA membrane wash of human lung fibroblast (LF) cultures. Incubation with human plasma (5% vol/vol) or purified FXa (15¿50 nM) evoked fibrogenic responses in LF cultures, with FXa increasing interleukin-6 (IL-6) production and cell number by 270 and 46%, respectively (P < 0.05, n = 5¿8). The fibrogenic actions of plasma or FXa were attenuated by the selective FXa inhibitor apixaban (10 µM, or antibodies raised against annexin A2 or PAR-1 (2 µg/ml). FXastimulated LFs from IPF patients (n = 6) produced twice as much IL-6 as controls (n = 10) (P < 0.05), corresponding with increased levels of extracellular annexin A2. Annexin A2 gene deletion in mice reduced bleomycin-induced increases in bronchoalveolar lavage fluid (BALF) IL-6 levels and cell number (*P < 0.05; n = 4¿12). Lung fibrogenic gene expression and dry weight were reduced by annexin A2 gene deletion, but lung levels of collagen were not. Our data suggest that annexin A2 contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa. Extracellular annexin A2 is a potential target for the treatment of IPF.

DOI 10.1152/ajplung.00553.2016
Co-authors Christopher Grainge, Darryl Knight
2016 Schuliga M, Royce SG, Langenbach S, Berhan A, Harris T, Keenan CR, Stewart AG, 'The coagulant factor Xa induces protease-activated receptor-1 and annexin A2-dependent airway smooth muscle cytokine production and cell proliferation', American Journal of Respiratory Cell and Molecular Biology, 54 200-209 (2016) [C1]

Copyright © 2016 by the American Thoracic Society. During asthma exacerbation, plasma circulating coagulant factor X (FX) enters the inflamed airways and is activated (FXa). FXa ... [more]

Copyright © 2016 by the American Thoracic Society. During asthma exacerbation, plasma circulating coagulant factor X (FX) enters the inflamed airways and is activated (FXa). FXa may have an important role in asthma, being involved in thrombin activation and an agonist of protease-activated receptor-1 (PAR-1). Extracellular annexin A2 and integrins are also implicated in PAR-1 signaling. In this study, the potential role of PAR-1 in mediating the effects of FXa on human airway smooth muscle (ASM) cell cytokine production and proliferation was investigated. FXa (5-50 nM), but not FX, stimulated increases in ASM IL-6 production and cell number after 24- and 48-hour incubation, respectively (P < 0.05; n = 5). FXa (15 nM) also stimulated increases in the levels of mRNA for cytokines (IL-6), cell cycle-related protein (cyclin D1), and proremodeling proteins (FGF-2, PDGF-B, CTGF, SM22, and P AI-1) after 3-hour incubation (P < 0.05; n = 4). The actions of FXa were insensitive to inhibition by hirudin (1 U/ml), a selective thrombin inhibitor, but were attenuated by SCH79797 (100 nM), a PAR-1 antagonist, or Cpd 22 (1 µM), an inhibitor of integrin-linked kinase. The selective targeting of PAR-1, annexin A2, or ß 1-integrin by small interfering RNA and/or by functional blocking antibodies also attenuated FXa-evoked responses. In contrast, the targeting of annexin A2 did not inhibit thrombin-stimulated ASM function. In airway biopsies of patients with asthma, FXa and annexin A2 were detected in the ASM bundle by immunohistochemistry. These findings establish FXa as a potentially important asthma mediator, stimulating ASM function through actions requiring PAR-1 and annexin A2 and involving integrin coactivation.

DOI 10.1165/rcmb.2014-0419OC
Citations Scopus - 4Web of Science - 4
2015 Keenan CR, Schuliga MJ, Stewart AG, 'Pro-inflammatory mediators increase levels of the noncoding RNA GAS5 in airway smooth muscle and epithelial cells', Canadian Journal of Physiology and Pharmacology, 93 203-206 (2015)

© 2015, National Research Council of Canada. All rights reserved. The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus... [more]

© 2015, National Research Council of Canada. All rights reserved. The long noncoding RNA (lncRNA) GAS5 has been found to act as a decoy for the glucocorticoid receptor (GR), thus implicating GAS5 as a potential regulator of glucocorticoid sensitivity and resistance. Airway smooth muscle (ASM) cells and airway epithelial cells (AEC) play an important role in the pathogenesis and persistence of asthma and other chronic airways diseases. These airway structural cell types are also important cellular targets of the anti-inflammatory actions of glucocorticoids. In this study, we sought to examine the relevance of GAS5 to glucocorticoid sensitivity and resistance in ASM and AEC. We provide the first evidence that pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in AEC.

DOI 10.1139/cjpp-2014-0391
Citations Scopus - 9
2015 Schuliga M, 'NF-kappaB Signaling in Chronic Inflammatory Airway Disease', BIOMOLECULES, 5 1266-1283 (2015)
DOI 10.3390/biom5031266
Citations Scopus - 51Web of Science - 43
2015 Schuliga M, 'The Inflammatory Actions of Coagulant and Fibrinolytic Proteases in Disease', MEDIATORS OF INFLAMMATION, (2015)
DOI 10.1155/2015/437695
Citations Scopus - 19Web of Science - 18
2014 Alkhouri H, Poppinga WJ, Tania NP, Ammit A, Schuliga M, 'Regulation of pulmonary inflammation by mesenchymal cells', Pulmonary Pharmacology and Therapeutics, 29 156e165 (2014)

© 2014 Elsevier Ltd. Pulmonary inflammation and tissue remodelling are common elements of chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD... [more]

© 2014 Elsevier Ltd. Pulmonary inflammation and tissue remodelling are common elements of chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and pulmonary hypertension (PH). In disease, pulmonary mesenchymal cells not only contribute to tissue remodelling, but also have an important role in pulmonary inflammation. This review will describe the immunomodulatory functions of pulmonary mesenchymal cells, such as airway smooth muscle (ASM) cells and lung fibroblasts, in chronic respiratory disease. An important theme of the review is that pulmonary mesenchymal cells not only respond to inflammatory mediators, but also produce their own mediators, whether pro-inflammatory or pro-resolving, which influence the quantity and quality of the lung immune response. The notion that defective pro-inflammatory or pro-resolving signalling in these cells potentially contributes to disease progression is also discussed. Finally, the concept of specifically targeting pulmonary mesenchymal cell immunomodulatory function to improve therapeutic control of chronic respiratory disease is considered.

DOI 10.1016/j.pupt.2014.03.001
Citations Scopus - 11Web of Science - 15
2013 Stewart AG, Xia YC, Harris T, Royce S, Hamilton JA, Schuliga M, 'Plasminogen-stimulated airway smooth muscle cell proliferation is mediated by urokinase and annexin A2, involving plasmin-activated cell signalling', British Journal of Pharmacology, 170 1421-1435 (2013) [C1]

Background and Purpose The conversion of plasminogen into plasmin by interstitial urokinase plasminogen activator (uPA) is potentially important in asthma pathophysiology. In this... [more]

Background and Purpose The conversion of plasminogen into plasmin by interstitial urokinase plasminogen activator (uPA) is potentially important in asthma pathophysiology. In this study, the effect of uPA-mediated plasminogen activation on airway smooth muscle (ASM) cell proliferation was investigated. Experimental Approach Human ASM cells were incubated with plasminogen (0.5-50 µg·mL -1 ) or plasmin (0.5-50 mU·mL -1 ) in the presence of pharmacological inhibitors, including UK122, an inhibitor of uPA. Proliferation was assessed by increases in cell number or MTT reduction after 48 h incubation with plasmin(ogen), and by earlier increases in [ 3 H]-thymidine incorporation and cyclin D1 expression. Key Results Plasminogen (5 µg·mL -1 )-stimulated increases in cell proliferation were attenuated by UK122 (10 µM) or by transfection with uPA gene-specific siRNA. Exogenous plasmin (5 mU·mL -1 ) also stimulated increases in cell proliferation. Inhibition of plasmin-stimulated ERK1/2 or PI3K/Akt signalling attenuated plasmin-stimulated increases in ASM proliferation. Furthermore, pharmacological inhibition of cell signalling mediated by the EGF receptor, a receptor trans-activated by plasmin, also reduced plasmin(ogen)-stimulated cell proliferation. Knock down of annexin A2, which has dual roles in both plasminogen activation and plasmin-signal transduction, also attenuated ASM cell proliferation following incubation with either plasminogen or plasmin. Conclusions and Implications Plasminogen stimulates ASM cell proliferation in a manner mediated by uPA and involving multiple signalling pathways downstream of plasmin. Targeting mediators of plasminogen-evoked ASM responses, such as uPA or annexin A2, may be useful in the treatment of asthma. © 2013 The British Pharmacological Society.

DOI 10.1111/bph.12422
Citations Scopus - 11Web of Science - 10
2013 Schuliga M, Langenbach S, Xia YC, Qin C, Mok JSL, Harris T, et al., 'Plasminogen-Stimulated Inflammatory Cytokine Production by Airway Smooth Muscle Cells Is Regulated by Annexin A2', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 49 751-758 (2013) [C1]
DOI 10.1165/rcmb.2012-0404OC
Citations Web of Science - 11
2013 Schuliga M, Javeed A, Harris T, Xia Y, Qin C, Wang Z, et al., 'Transforming growth factor-ß-Induced differentiation of airway smooth muscle cells is inhibited by fibroblast growth factor-2', American Journal of Respiratory Cell and Molecular Biology, 48 346-353 (2013) [C1]

In asthma, basic fibroblast growth factor (FGF-2) plays an important (patho)physiological role. This study examines the effects of FGF-2 on the transforming growth factor-b (TGF-b... [more]

In asthma, basic fibroblast growth factor (FGF-2) plays an important (patho)physiological role. This study examines the effects of FGF-2 on the transforming growth factor-b (TGF-b)-stimulated differentiation of airway smooth muscle (ASM) cells in vitro. The differentiation of humanASMcells after incubation with TGF-b(100 pM)and/ or FGF-2 (300 pM) for 48 hours was assessed by increases in contractile protein expression, actin-cytoskeleton reorganization, enhancements in cell stiffness, and collagen remodeling. FGF-2 inhibited TGF-ß-stimulated increases in transgelin (SM22) and calponin gene expression (n = 15, P < 0.01) in an extracellular signal-regulated kinase 1/2 (ERK1/2) signal transduction-dependent manner. The abundance of ordered a-smooth muscle actin (a-SMA) filaments formed in the presence of TGF-b were also reduced by FGF-2, as was the ratio of F-actin to G-actin (n = 8, P < 0.01). Furthermore, FGF-2 attenuated TGF-ß-stimulated increases in ASM cell stiffness andtheASM-mediatedcontraction of lattices,composed of collagen fibrils (n = 5, P < 0.01). However, the TGF-ß-stimulated production of IL-6 was not influenced by FGF-2 (n=4, P. > .05), suggesting that FGF-2 antagonism is selective for the regulation of ASM cell contractile protein expression, organization, and function. Another mitogen, thrombin (0.3 U ml21), exerted no effect on TGF-ß-regulated contractile protein expression (n=8, P. > .05),a-SMA organization, or the ratio of F-actin to G-actin (n=4, P. > .05), suggesting that the inhibitory effect of FGF-2 is dissociated from its mitogenic actions. The addition of FGF-2, 24 hours after TGF-b treatment, still reduced contractile protein expression, even when the TGF-ß-receptor kinase inhibitor, SB431542 (10 mM), was added 1 hour before FGF-2. Weconclude that the ASM cell differentiation promoted by TGF-b is antagonized by FGF-2. A better understanding of the mechanism of action for FGF-2 is necessary to develop a strategy for therapeutic exploitation in the treatment of asthma. Copyright © 2013 by the American Thoracic Society.

DOI 10.1165/rcmb.2012-0159OC
Citations Scopus - 19
2013 Schuliga M, Langenbach S, Xia YC, Qin C, Mok JSL, Harris T, et al., 'Plasminogen-stimulated inflammatory cytokine production by airway smooth muscle cells is regulated by annexin A2', American Journal of Respiratory Cell and Molecular Biology, 49 751-758 (2013)

Plasminogen has a role in airway inflammation. Airway smooth muscle(ASM) cells cleave plasminogen into plasmin, a protease with proinflammatory activity. In this study, the effect... [more]

Plasminogen has a role in airway inflammation. Airway smooth muscle(ASM) cells cleave plasminogen into plasmin, a protease with proinflammatory activity. In this study, the effect of plasminogen on cytokine production by human ASM cells was investigated in vitro. Levels of IL-6 and IL-8 in the medium of ASM cells were increased byincubation with plasminogen (5-50 µg/ml) for 24 hours (P,0.05; n = 6-9), corresponding to changes in the levels of cytokine mRNA at 4 hours. The effects of plasminogen were attenuated by a2- antiplasmin (1 mg/ml), a plasmin inhibitor (P < 0.05; n = 6-12). Exogenous plasmin (5-15 mU/ml) also stimulated cytokine production (P < 0.05; n = 6-8) in a manner sensitive to serine-protease inhibition by aprotinin (10 KIU/ml). Plasminogen-stimulated cytokine production was increased in cells pretreated with basic fibroblast growth factor (300 pM) in a manner associated with increases in urokinase plasminogen activator expression and plasmin formation. The knockdown of annexin A2, a component of the putative plasminogen receptor comprised of annexin A2 and S100A10, attenuated plasminogen conversion into plasmin and plasmin-stimulated cytokine production byASMcells. Moreover, a role for annexin A2 in airway inflammation was demonstrated in annexin A2-/- mice in which antigen-induced increases in inflammatory cell number and IL-6 levels in the bronchoalveolar lavage fluid were reduced (P < 0.01; n = 10-14). In conclusion, plasminogen stimulates ASM cytokine production in a manner regulated by annexin A2. Our study shows for the first time that targeting annexin A2-mediated signaling may provide a novel therapeutic approach to the treatment of airway inflammation in diseases such as chronic asthma. Copyright © 2013 by the American Thoracic Society.

DOI 10.1165/rcmb.2012-0404OC
Citations Scopus - 9
2013 Schuliga M, Westall G, Xia Y, Stewart AG, 'The plasminogen activation system: New targets in lung inflammation and remodeling', Current Opinion in Pharmacology, 13 386-393 (2013) [C1]

The plasminogen activation system (PAS) and the plasmin it forms have dual roles in chronic respiratory diseases including asthma, chronic obstructive pulmonary disease and inters... [more]

The plasminogen activation system (PAS) and the plasmin it forms have dual roles in chronic respiratory diseases including asthma, chronic obstructive pulmonary disease and interstitial lung disease. Whilst plasmin-mediated airspace fibrinolysis is beneficial, interstitial plasmin contributes to lung dysfunction because of its pro-inflammatory and tissue remodeling activities. Recent studies highlight the potential of fibrinolytic agents, including small molecule inhibitors of plasminogen activator inhibitor-1 (PAI-1), as treatments for chronic respiratory disease. Current data also suggest that interstitial urokinase plasminogen activator is an important mediator of lung inflammation and remodeling. However, further preclinical characterization of uPA as a drug target for lung disease is required. Here we review the concept of selectively targeting the contributions of PAS to treat chronic respiratory disease. © 2013 Elsevier Ltd. All rights reserved.

DOI 10.1016/j.coph.2013.05.014
Citations Scopus - 23Web of Science - 23
2012 Salem S, Harris T, Mok JSL, Li MYS, Keenan CR, Schuliga MJ, Stewart AG, 'Transforming growth factor-ß impairs glucocorticoid activity in the A549 lung adenocarcinoma cell line', British Journal of Pharmacology, 166 2036-2048 (2012) [C1]
DOI 10.1111/j.1476-5381.2012.01885.x
Citations Scopus - 24Web of Science - 29
Co-authors Saad Salem
2011 Khau T, Langenbach SY, Schuliga M, Harris T, Johnstone CN, Anderson RL, Stewart AG, 'Annexin-1 signals mitogen-stimulated breast tumor cell proliferation by activation of the formyl peptide receptors (FPRs) 1 and 2', FASEB Journal, 25 483-496 (2011) [C1]
DOI 10.1096/fj.09-154096
Citations Scopus - 46Web of Science - 44
2011 Xia YC, Schuliga M, Shepherd M, Powell M, Harris T, Langenbach SY, et al., 'Functional expression of IgG-Fc receptors in human airway smooth muscle cells', American Journal of Respiratory Cell and Molecular Biology, 44 665-672 (2011) [C1]
DOI 10.1165/rcmb.2009-0371OC
Citations Scopus - 13Web of Science - 12
2011 Schuliga M, Harris T, Stewart AG, 'Plasminogen activation by airway smooth muscle is regulated by type I collagen', American Journal of Respiratory Cell and Molecular Biology, 44 831-839 (2011) [C1]
DOI 10.1165/rcmb.2009-0469OC
Citations Scopus - 10Web of Science - 11
2011 Shand FHW, Langenbach SY, Keenan CR, Ma SP, Wheaton BJ, Schuliga MJ, et al., 'In vitro and in vivo evidence for anti-inflammatory properties of 2-methoxyestradiol', Journal of Pharmacology and Experimental Therapeutics, 336 962-972 (2011) [C1]
DOI 10.1124/jpet.110.174854
Citations Scopus - 16Web of Science - 17
2010 Schuliga M, Ong SC, Soon L, Zal F, Harris T, Stewart AG, 'Airway smooth muscle remodels pericellular collagen fibrils: implications for proliferation', AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 298 L584-L592 (2010)
DOI 10.1152/ajplung.00312.2009
Citations Scopus - 23Web of Science - 21
2009 Burgess JK, Ceresa C, Johnson SR, Kanabar V, Moir LM, Nguyen TTB, et al., 'Tissue and matrix influences on airway smooth muscle function', PULMONARY PHARMACOLOGY & THERAPEUTICS, 22 379-387 (2009)
DOI 10.1016/j.pupt.2008.12.007
Citations Scopus - 35Web of Science - 30
2009 Schuliga MJ, See I, Ong SC, Soon L, Camoretti-Mercado B, Harris T, Stewart AG, 'Fibrillar collagen clamps lung mesenchymal cells in a nonproliferative and noncontractile phenotype', American Journal of Respiratory Cell and Molecular Biology, 41 731-741 (2009)

Pulmonary fibrosis is characterized by phenotypic changes to mesenchymal cells and an increase in the deposition of fibrillar collagen (f Collagen). This study investigated the ef... [more]

Pulmonary fibrosis is characterized by phenotypic changes to mesenchymal cells and an increase in the deposition of fibrillar collagen (f Collagen). This study investigated the effect of type I fCollagen on the phenotypic plasticity of human parenchymal fibroblasts (PFbs) in vitro. Cell numbers were45%lower whencultured on fCollagen as compared with culture on its degradation product, monomeric collagen (mCollagen). DNA profiles indicated that fCollagen is antiproliferative, rather than proapoptotic. fCollagen suppressed basic fibroblast growth factor-stimulated increases in the levels of cyclin E and CDK2 mRNA. fCollagen also suppressed transforming growth factor-ß (100 pM)-stimulated increases in the mRNA and protein levels of a-smooth muscle actin (a-SMA), a marker of the myofibroblast phenotype. However, in cells exposed to f Collagen, the levels of matrix metalloproteinase (MMP)-1 and -14 mRNA, as well as active MMP-2 protein, were increased by between two- and fivefold. The MMP inhibitors, ilomastat (10 µM) and doxycycline (30 µM), attenuated the dissolution of collagen fibrils by fibroblasts maintained on fCollagen, with a corresponding decrease in cell number. Ilomastat also reduced a-SMA expression and the capacity of PFb to contract three-dimensional fCollagen gels. Thus, exposure of fibroblasts to the fibrillar form of type I collagen in vitro reduces cell proliferation, increases MMP production and activation, and attenuates differentiation of PFb into myofibroblasts. fCollagen appears to apply a phenotypic clamp on lung fibroblasts that may be partially released by autocrine MMP activity.

DOI 10.1165/rcmb.2008-0361OC
Citations Scopus - 20
2009 Stewart AG, Schuliga M, Harris T, Che W, 'Interactions between the Inflammation and Coagulation Systems in Airway Wall Remodelling: Plasminogen-Evoked Fibroblast Collagen Gel Contraction', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 179 (2009)
2007 Sutherland TE, Anderson RL, Hughes RA, Altmann E, Schuliga M, Ziogas J, Stewart AG, '2-methoxyestradiol - a unique blend of activities generating a new class of anti-tumour/anti-inflammatory agents', DRUG DISCOVERY TODAY, 12 577-584 (2007)
DOI 10.1016/j.drudis.2007.05.005
Citations Scopus - 70Web of Science - 59
2007 Shepherd MC, Duffy SM, Harris T, Cruse G, Schuliga M, Brightling CE, et al., 'K(Ca)3.1 Ca2+-Activated K+ channels regulate human airway smooth muscle proliferation', AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 37 525-531 (2007)
DOI 10.1165/rcmb.2006-03580C
Citations Web of Science - 58
2007 Shepherd MC, Duffy SM, Harris T, Cruse G, Schuliga M, Brightling CE, et al., 'K

Airway smooth muscle cell hyperplasia contributes to airway remodeling and hyperreactivity characteristic of asthma. Changes to potassium channel activity in proliferating human a... [more]

Airway smooth muscle cell hyperplasia contributes to airway remodeling and hyperreactivity characteristic of asthma. Changes to potassium channel activity in proliferating human airway smooth muscle (HASM) cells have been described, but no regulatory role in proliferation has been attributed to them. We sought to investigate the expression of the intermediate conductance calcium-activated potassium channel K Ca 3.1 in HASM cells and investigate its role in proliferation. Smooth muscle cells derived from human airways were grown in vitro and K Ca 3.1 channel expression was measured using Western blot, RT-PCR, and patch clamp electrophysiology. Pharmacologic inhibitors of the channel were used in assays of cellular proliferation, and flow cytometry was used to identify cell cycle regulation. HASM cells expressed K Ca 3.1 channel mRNA, protein, and activity with up-regulation evident after transforming growth factor-ß stimulation. Pharmacologic inhibition of K Ca 3.1 led to growth arrest in cells stimulated to proliferate with mitogens. These inhibitors did not cause cellular toxicity or induce apoptosis. We have demonstrated, for the first time, the expression of K Ca 3.1 channels in HASM cells. In addition, we have shown that K Ca 3.1 channels are important in HASM cell proliferation, making these channels a potential therapeutic target in airway remodeling.

DOI 10.1165/rcmb.2006-0358OC
Citations Scopus - 59
2006 Bonacci JV, Schuliga M, Harris T, Stewart AG, 'Collagen impairs glucocorticoid actions in airway smooth muscle through integrin signalling', BRITISH JOURNAL OF PHARMACOLOGY, 149 365-373 (2006)
DOI 10.1038/sj.bjp.0706881
Citations Scopus - 42Web of Science - 38
2005 Tran T, Fernandes DJ, Schuliga M, Harris T, Landells L, Stewart AG, 'Stimulus-dependent glucocorticoid-resistance of GM-CSF production in human cultured airway smooth muscle', BRITISH JOURNAL OF PHARMACOLOGY, 145 123-131 (2005)
DOI 10.1038/sj.bjp.0706174
Citations Scopus - 27Web of Science - 24
2005 Johansson PA, Dziegielewska KM, Ek CJ, Habgood MD, Mollgard K, Potter A, et al., 'Aquaporin-1 in the choroid plexuses of developing mammalian brain', CELL AND TISSUE RESEARCH, 322 353-364 (2005)
DOI 10.1007/s00441-005-1120-x
Citations Scopus - 44Web of Science - 42
2005 Sutherland TE, Schuliga M, Harris T, Eckhardt BL, Anderson RL, Quan L, Stewart AG, '2-methoxyestradiol is an estrogen receptor agonist that supports tumor growth in murine xenograft models of breast cancer', CLINICAL CANCER RESEARCH, 11 1722-1732 (2005)
DOI 10.1158/1078-0432.CCR-04-1789
Citations Scopus - 35Web of Science - 35
2005 Stewart A, Sutherland TE, Schuliga M, Harris T, Quan L, McAllister D, et al., 'The potential and suitability of 2-methoxyestradiol in cancer therapy - Response', CLINICAL CANCER RESEARCH, 11 6095-6096 (2005)
Citations Web of Science - 1
2005 Sidor C, D'Amato R, Miller KD, Stewart A, Sutherland TE, Schuliga M, et al., 'The potential and suitability of 2-methoxyestradiol in cancer therapy (multiple letters)', Clinical Cancer Research, 11 6094-6096 (2005)
DOI 10.1158/1078-0432.CCR-05-0724
Citations Scopus - 9
2002 Schuliga M, Chouchane S, Snow ET, 'Upregulation of glutathione-related genes and enzyme activities in cultured human cells by sublethal concentrations of inorganic arsenic', TOXICOLOGICAL SCIENCES, 70 183-192 (2002)
DOI 10.1093/toxsci/70.2.183
Citations Scopus - 111Web of Science - 109
Show 29 more journal articles

Conference (34 outputs)

Year Citation Altmetrics Link
2017 Waters DW, Schuliga M, Fogarty E, Burgess JK, Grainge C, Westall G, et al., 'Dysregulated Stat3 Signaling Induces And Reinforces Fibroblast Senescence In Lung Fibroblasts Of Ipf Patients', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Darryl Knight, Christopher Grainge
2017 Schuliga M, Jaffar J, Berhan A, Langenbach S, Waters DW, Harris T, et al., 'Annexin A2 Mediates Fibrogenic Actions Of Factor Xa On Lung Fibroblasts: A Potential Role In Lung Injury And Fibrosis', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Darryl Knight
2017 Fogarty E, Waters D, Grainge C, Burgess JK, Prele CM, Laurent G, et al., 'Senescent Lung Fibroblasts Reduce Alveolar Epithelial Cell Number In Co-Culture', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Darryl Knight, Christopher Grainge
2017 Schuliga M, Pechkovsky DV, Waters D, Fogarty E, Hogaboam CM, Yao E, et al., 'LUNG FIBROBLASTS OF IPF PATIENTS DISPLAY SENESCENCE-LIKE FEATURES IN VITRO', RESPIROLOGY (2017)
Co-authors Christopher Grainge, Darryl Knight
2017 Waters DW, Schuliga M, Fogarty E, Burgess J, Grainge C, Westall G, et al., 'DYSREGULATED STAT3 SIGNALING INDUCES AND REINFORCES FIBROBLAST SENESCENCE IN LUNG FIBROBLASTS OF IPF PATIENTS', RESPIROLOGY (2017)
Co-authors Darryl Knight, Christopher Grainge
2016 Jaffar J, Symons K, Goh N, O'Hehir R, Schuliga M, Stewart AG, et al., 'Serum Matrix Metalloproteinase-7 Is A Potential Marker Of Active Disease In Patients With Idiopathic Pulmonary Fibrosis', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2016)
2016 Schuliga M, Jaffar J, Berhan A, Langenbach S, Harris T, Westall G, Stewart AG, 'Urokinase Plasminogen Activator (upa) Is Increased In Interstitial Lung Disease (ild): A Potential Fibrogenic Mediator And Biomarker In Ild', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2016)
2016 Stewart AG, Jativa FR, Schuliga M, Wang Z, Harris T, Jaffar J, et al., 'Increased Stiffness And Changes In Tgfbeta-Induced Gene Expression In Lung Fibroblast Spheroids From Ipf Fibroblasts', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Francisco, CA (2016)
2016 Jaffar J, Symons K, Goh N, O'Hehir R, Schuliga M, Stewart A, et al., 'SERUM MMP7 IS INCREASED IN PATIENTS WITH PROGRESSIVE IDIOPATHIC PULMONARY FIBROSIS', RESPIROLOGY (2016)
2014 Schuliga M, Harris T, Royce S, Stewart A, 'The coagulant factor Xa induces PAR-1 and annexin A2-dependent airway smooth muscle cytokine production and cell proliferation', EUROPEAN RESPIRATORY JOURNAL (2014)
2014 Meurs H, Minovic I, Harris T, Xia YC, Schuliga M, Gosens R, et al., 'Potential Role For Chondrocytes In Airway Remodeling', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
2014 Schuliga M, Xia Y, Langenbach S, Harris T, Stewart AG, 'Extracellular Annexin A2 Mediates Lung Fibroblast Cytokine Production And Proliferation: A Potential Role In Pulmonary Fibrosis', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2014)
2014 Schuliga M, Langenbach S, Xia Y, Harris T, Stewart A, 'EXTRACELLULAR ANNEXIN A2 MEDIATES INFLAMMATORY AND FIBRO-PROLIFERATIVE RESPONSES IN MODELS OF PULMONARY FIBROSIS', RESPIROLOGY (2014)
2013 Keenan CR, Salem S, Harris T, Schuliga M, Stewart AG, 'Transforming Growth Factor-beta Induces Glucocorticoid Resistance In Human Bronchial Epithelial Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Schuliga M, Harris T, Xia YC, Wang Z, Zhang X, Srinivason V, et al., 'Fgf-2 Modulates Human Airway Smooth Muscle Contractile Protein Expression And Cell Stiffness In A Reversible, Smad-Independent Manner', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Schuliga M, Xia YC, Harris T, Stewart AG, 'Plasminogen-Stimulated Airway Smooth Muscle Cell Proliferation Is Mediated By Urokinase And Involves Plasmin-Activated Cell Signaling', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
2013 Schuliga M, Harris T, Xia Y, Wang Z, Zhang X, Lee P, Stewart A, 'FGF-2 modulates human airway smooth muscle contractile protein expression and cell stiffness', EUROPEAN RESPIRATORY JOURNAL (2013)
2013 Keenan C, Lopez-Campos G, Salem S, Harris T, Schuliga M, Johnstone C, Stewart A, 'RNA-seq analysis of transforming growth factor-beta-induced glucocorticoid resistance in human bronchial epithelial cells', EUROPEAN RESPIRATORY JOURNAL (2013)
Co-authors Saad Salem
2013 Keenan CR, Salem S, Harris T, Schuliga M, Stewart AG, 'TRANSFORMING GROWTH FACTOR-beta INDUCES GLUCOCORTICOID RESISTANCE IN HUMAN BRONCHIAL EPITHELIAL CELLS', RESPIROLOGY (2013)
Co-authors Saad Salem
2013 Schuliga M, Javeed A, Harris T, Xia Y, Qin C, Wang Z, et al., 'Transforming growth factor-ß-induced differentiation of airway smooth muscle cells is inhibited by fibroblast growth factor-2.', Am J Respir Cell Mol Biol, United States (2013)
DOI 10.1165/rcmb.2012-0151OC
Citations Web of Science - 19
2012 Schuliga M, Che WC, Harris T, Stewart AG, 'PLASMINOGEN EVOKES EXTRACELLULAR MATRIX REMODELLING BY HUMAN AIRWAY FIBROBLASTS', RESPIROLOGY (2012)
2012 Schuliga M, Javeed A, Harris T, Stewart AG, 'TGF-[BETA]-STIMULATED DIFFERENTIATION OF AIRWAY SMOOTH MUSCLE CELLS IS INHIBITED BY FGF-2', RESPIROLOGY (2012)
2011 Salem S, Harris T, Schuliga M, Mok J, Stewart A, 'Transforming Growth Factor Beta (TGFBeta) Induces Glucocorticoid-Resistance In A549 Adenocarcinoma Cell Line By Reducing Glucocorticoid Receptor Nuclear Localisation', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2011)
Co-authors Saad Salem
2011 Schuliga M, Zal F, Qin C, Harris T, Stewart A, 'Plasmin Stimulates Airway Smooth Muscle Cells To Proliferate And Produce Interleukin-6', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2011)
2010 Schuliga M, Harris T, Stewart A, 'Plasmin Formation By Airway Smooth Muscle Is Accelerated By Culture On Fibrillar Type 1 Collagen', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2010)
2010 Schuliga M, Harris T, Stewart A, 'Transforming Growth Factor Beta Regulates Plasminogen Activation By Airway Smooth Muscle', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2010)
2010 Stewart A, Salem S, Lian JMS, Schuliga M, Harris T, 'Glucocorticoid resistance in human airway epithelial cells: a potential role for Transforming Growth Factor-beta', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2010)
Co-authors Saad Salem
2009 Stewart AG, Schuliga M, Mok J, Salem S, Harris T, 'TGF-Induces Glucocorticoid Resistance beta.', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
Co-authors Saad Salem
2009 Schuliga M, Soon L, See I, Harris T, Stewart AG, 'Loss of Fibrillar Collagen Releases an Anti-Fibrotic Clamp on Parenchymal Fibroblasts.', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
2009 Xia YC, Schuliga M, Shepherd M, Harris T, Stewart AG, Mackay GA, 'Inhibitory IgG Fc Receptor Fc gamma RIIb Expression and Activity in Human Airway Smooth Muscle Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
2009 Schuliga M, Mok J, Zal F, Harris T, Stewart AG, 'Airway Smooth Muscle Activation of Plasminogen: Functional Effects and Dependence on the Annexin II Tetramer', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
2009 Shand FHW, Langenbach SY, Ma SP, Wheaton BJ, Leung B, Harris T, et al., 'The Endogenous Estrogen Metabolite 2-Methoxyestradiol: Prototype for a New Class of Anti-Inflammatory Agents.', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
2008 Khau T, Schuliga M, Harris T, Stewart A, 'Annexin I regulation of breast cancer cell proliferation', EJC SUPPLEMENTS, Geneva, SWITZERLAND (2008)
DOI 10.1016/S1359-6349(08)72309-7
Citations Web of Science - 1
2007 Langenbach SY, Wheaton BJ, Fernandes DJ, Jones C, Sutherland TE, Wraith BC, et al., 'Resistance of fibrogenic responses to glucocorticoid and 2-methoxyestradiol in bleomycin-induced lung fibrosis in mice', Canadian Journal of Physiology and Pharmacology (2007)

Bleomycin-induced lung fibrosis in mice reproduces some key features of pulmonary fibrosis in humans including alveolar inflammation, myofibroblast proliferation, and collagen dep... [more]

Bleomycin-induced lung fibrosis in mice reproduces some key features of pulmonary fibrosis in humans including alveolar inflammation, myofibroblast proliferation, and collagen deposition. Glucocorticoids have been used as first-line therapy for the treatment of lung fibrosis, although their clinical efficacy is equivocal. We examined the effect of the glucocorticoid, methylprednisolone (MP), and the estrogen metabolite, 2-methoxyestradiol (2MEO) on bleomycin-induced bronchoalveolar inflammation, fibrosis, and changes in lung function. The characterization of the time-course of the bleomycin-induced fibrosis indicated that lung dry mass and hydroxyproline content showed less variance than histopathological assessment of fibrosis. The bleomycin-induced increases in bronchoalveolar lavage (BAL) fluid cell number and protein levels w ere not significantly influenced by treatment with either MP (1 mg·(kg body mass) -1 ·day -1 , i.p.) or 2MEO (50 mg·(kg body mass) -1 ·day -1 , i.p.). Lung fibrosis, measured histopathologically or by hydroxyproline content, was not significantly influenced by either MP or 2MEO treatment, whereas the latter agent did reduce the increment in lung dry mass. The enlargement of alveolar airspaces and the decline in lung compliance were exacerbated by MP treatment. These data suggest that bleomycin-induced pulmonary fibrosis is resistant to inhibition by concurrent treatment with either glucocorticoids or 2MEO. © 2007 NRC.

DOI 10.1139/Y07-065
Citations Scopus - 14
Show 31 more conferences
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Grants and Funding

Summary

Number of grants 8
Total funding $1,228,200

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


20173 grants / $45,000

Mechano-transduction signaling complexes of urokinase and its receptor in lung fibrosis: A potential target for idiopathic pulmonary fibrosis (IPF)$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Michael Schuliga, Conjoint Associate Professor Christopher Grainge, Professor Darryl Knight
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700697
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Mechano-transduction signalling complexes of urokinase and it receptor in lung fibrosis: A potential target for idiopathic pulmonary fibrosis (IPF)$20,000

Funding body: John Hunter Charitable Trust Grant

Funding body John Hunter Charitable Trust Grant
Project Team

Dr Michael Schuliga (CIA), A/Prof Chris Grainge (CIB) & Prof Darryl Knight (CIC)

Scheme John Hunter Charitable Trust Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON N

Annexin A2 in IPF and potential as novel therapeutic target $5,000

Funding body: Lung Foundation Australia

Funding body Lung Foundation Australia
Scheme Research Award
Role Lead
Funding Start 2017
Funding Finish 2018
GNo
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON N

20151 grants / $43,700

Effect of biomechanical strain on lung fibroblast function$43,700

Funding body: Faculty of Medicine, Dental and Health Sciences

Funding body Faculty of Medicine, Dental and Health Sciences
Project Team

Dr Michael Schuliga

Scheme Research Grant Support Scheme
Role Lead
Funding Start 2015
Funding Finish 2016
GNo
Type Of Funding External
Category EXTE
UON N

20131 grants / $536,500

Airway smooth muscle and fixed airway obstruction: strategies for softening muscle $536,500

APP1045372

To investigate the inhibitory effect of FGF-2 on ASM cell hypertrophy and cell stiffness, and to test the validity of using FGF-2 mechanism selective-analogues in the treatment of airway obstruction in asthma. 

Funding body: National Health & Medical Research Council of Australia (NH&MRC)

Funding body National Health & Medical Research Council of Australia (NH&MRC)
Project Team

Pfor Alastair Stewart (CIA), Dr Michael Schuliga (CIB), Prof Peter Lee (CIC) and Dr Xuehua Zhang (CID)

Scheme Project Grant
Role Investigator
Funding Start 2013
Funding Finish 2015
GNo
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON N

20121 grants / $538,000

Urokinase is a key mediator of airway inflammation and tissue remodelling in asthma$538,000

APP1022048

To investigate the role of urokinase (uPA) in airway inflammation and tissue remodelling, and determine whether uPA is a therapeutic target for asthma. 

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team

Dr Michael Schuliga (CIA), Prof Alastair Stewart (CIB) and Dr. Lilian Soon (CIC)

Scheme Project Grant
Role Lead
Funding Start 2012
Funding Finish 2014
GNo
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON N

20092 grants / $65,000

Fibrinolysis in acute lung injury: validation of annexin A2 as a novel drug target$40,000

Funding body: CASS Foundation

Funding body CASS Foundation
Project Team

Prof Alastair Stewart and Dr Michael Schuliga

Scheme Scientific Grants
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

Non-fibrinolytic roles for plasmin in asthmatic airways remodelling$25,000

Funding body: Asthma Foundation of Victoria

Funding body Asthma Foundation of Victoria
Project Team

Dr Michael Schuliga

Scheme Helen Macpherson Smith Trust Award
Role Lead
Funding Start 2009
Funding Finish 2009
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N
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Research Supervision

Number of supervisions

Completed1
Current5

Total current UON EFTSL

PhD0.65

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD An Investigation of Regional Heterogeneity of the Pulmonary Microenvironment in Idiopathic Pulmonary Fibrosis PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Fibroblast Senescence as a Driver of Idiopathic Pulmonary Fibrosis PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD Fibroblast Senescence as a Driver of Idiopathic Pulmonary Fibrosis PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 Honours The role of coagulant proteases in chronic lung disease Pharmacology, The University of Melbourne Co-Supervisor
2014 PhD The role of coagulant proteases in chronic lung disease Medical Science, The University of Melbourne Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2013 PhD Transforming growth factor-β impairs glucocorticoid activity in airway epithelial cells Pharmacology, The University of Melbourne Co-Supervisor
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Dr Michael Schuliga

Position

Post-Doctoral Fellow
Knight Group
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email michael.schuliga@newcastle.edu.au
Phone (02) 40420845

Office

Building HMRI
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