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
  • lung disease
  • pharmacology
  • Senescence
  • fibroblasts
  • tissue remodelling
  • Urokinase plasminogen activator

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 - 4
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 (34 outputs)

Year Citation Altmetrics Link
2018 Waters DW, Blokland KEC, Pathinayake PS, Burgess JK, Mutsaers SE, Prele CM, et al., 'Fibroblast senescence in the pathology of idiopathic pulmonary fibrosis', American Journal of Physiology - Lung Cellular and Molecular Physiology, 315 L162-L172 (2018) [C1]

© 2018 American Physiological Society. All rights reserved. Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneu monia of unknown cause with a median survi... [more]

© 2018 American Physiological Society. All rights reserved. Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing interstitial pneu monia of unknown cause with a median survival of only three years. Little is known about the mechanisms that precede the excessive collagen deposition seen in IPF, but cellular senescence has been strongly implicated in disease pathology. Senescence is a state of irreversible cell-cycle arrest accompanied by an abnormal secretory profile and is thought to play a critical role in both development and wound repair. Normally, once a senescent cell has contributed to wound repair, it is promptly removed from the environment via infiltrating immune cells. However, if immune clearance fails, the persistence of senescent cells is thought to drive disease pathology through their altered secretory profile. One of the major cell types involved in wound healing is fibroblasts, and senescent fibroblasts have been identified in the lungs of patients with IPF and in fibroblast cultures from IPF lungs. The question of what is driving abnormally high numbers of fibroblasts into senescence remains unanswered. The transcription factor signal transducer and activator of transcription 3 (STAT3) plays a role in a myriad of processes, including cell-cycle progression, gene transcription, as well as mitochondrial respiration, all of which are dysregulated during senescence. Activation of STAT3 has previously been shown to correlate with IPF progression and therefore is a potential molecular target to modify early-stage senescence and restore normal fibroblast function. This review summarizes what is presently known about fibroblast senescence in IPF and how STAT3 may contribute to this phenotype.

DOI 10.1152/ajplung.00037.2018
Citations Scopus - 1Web of Science - 1
Co-authors Christopher Grainge, Darryl Knight
2018 Schuliga M, Grainge C, Westall G, Knight D, 'The fibrogenic actions of the coagulant and plasminogen activation systems in pulmonary fibrosis', International Journal of Biochemistry and Cell Biology, 97 108-117 (2018) [C1]

© 2018 Elsevier Ltd Fibrosis causes irreversible damage to lung structure and function in restrictive lung diseases such as idiopathic pulmonary fibrosis (IPF). Extravascular coag... [more]

© 2018 Elsevier Ltd Fibrosis causes irreversible damage to lung structure and function in restrictive lung diseases such as idiopathic pulmonary fibrosis (IPF). Extravascular coagulation involving fibrin formation in the intra-alveolar compartment is postulated to have a pivotal role in the development of pulmonary fibrosis, serving as a provisional matrix for migrating fibroblasts. Furthermore, proteases of the coagulation and plasminogen activation (plasminergic) systems that form and breakdown fibrin respectively directly contribute to pulmonary fibrosis. The coagulants, thrombin and factor Xa (FXa) evoke fibrogenic effects via cleavage of the N-terminus of protease-activated receptors (PARs). Whilst the formation and activity of plasmin, the principle plasminergic mediator is suppressed in the airspaces of patients with IPF, localized increases are likely to occur in the lung interstitium. Plasmin-evoked proteolytic activation of factor XII (FXII), matrix metalloproteases (MMPs) and latent, matrix-bound growth factors such as epidermal growth factor (EGF) indirectly implicate plasmin in pulmonary fibrosis. Another plasminergic protease, urokinase plasminogen activator (uPA) is associated with regions of fibrosis in the remodelled lung of IPF patients and elicits fibrogenic activity via binding its receptor (uPAR). Plasminogen activator inhibitor-1 (PAI-1) formed in the injured alveolar epithelium also contributes to pulmonary fibrosis in a manner that involves vitronectin binding. This review describes the mechanisms by which components of the two systems primarily involved in fibrin homeostasis contribute to interstitial fibrosis, with a particular focus on IPF. Selectively targeting the receptor-mediated mechanisms of coagulant and plasminergic proteases may limit pulmonary fibrosis, without the bleeding complications associated with conventional anti-coagulant and thrombolytic therapies.

DOI 10.1016/j.biocel.2018.02.016
Co-authors Darryl Knight, Christopher Grainge
2018 Keenan CR, Langenbach SY, Jativa F, Harris T, Li M, Chen Q, et al., 'Casein kinase 1d/e inhibitor, PF670462 attenuates the fibrogenic effects of transforming growth factor-ß in pulmonary fibrosis', Frontiers in Pharmacology, 9 (2018)

© 2018 Keenan, Langenbach, Jativa, Harris, Li, Chen, Xia, Gao, Schuliga, Jaffar, Prodanovic, Tu, Berhan, Lee, Westall and Stewart. Transforming growth factor-beta (TGF-ß) is a maj... [more]

© 2018 Keenan, Langenbach, Jativa, Harris, Li, Chen, Xia, Gao, Schuliga, Jaffar, Prodanovic, Tu, Berhan, Lee, Westall and Stewart. Transforming growth factor-beta (TGF-ß) is a major mediator of fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). However, therapeutic global inhibition of TGF-ß is limited by unwanted immunosuppression and mitral valve defects. We performed an extensive literature search to uncover a little-known connection between TGF-ß signaling and casein kinase (CK) activity. We have examined the abundance of CK1 delta and epsilon (CK1d/e) in lung tissue from IPF patients and non-diseased controls, and investigated whether inhibition of CK1d/e with PF670462 inhibits pulmonary fibrosis. CK1d/e levels in lung tissue from IPF patients and non-diseased controls were assessed by immunohistochemistry. Anti-fibrotic effects of the CK1d/e inhibitor PF670462 were assessed in pre-clinical models, including acute and chronic bleomycin mouse models and in vitro experiments on spheroids made from primary human lung fibroblast cells from IPF and control donors, and human A549 alveolar-like adenocarcinoma-derived epithelial cells. Increased expression of CK1d and e in IPF lungs compared to non-diseased controls was accompanied by increased levels of the product, phospho-period 2. In vitro, PF670462 prevented TGF-ß-induced epithelial-mesenchymal transition. The stiffness of IPF-derived spheroids was reduced by PF670462 and TGF-ß-induced fibrogenic gene expression was inhibited. The CK1d/e inhibitor PF670462 administered systemically or locally by inhalation prevented both acute and chronic bleomycin-induced pulmonary fibrosis in mice. PF670462 administered in a 'therapeutic' regimen (day 7 onward) prevented bleomycin-induced lung collagen accumulation. Elevated expression and activity of CK1d and e in IPF and anti-fibrogenic effects of the dual CK1d/e inhibitor, PF670462, support CK1d/e as novel therapeutic targets for IPF.

DOI 10.3389/fphar.2018.00738
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 1-15 (2017) [C1]
DOI 10.3389/fphys.2017.00777
Citations Scopus - 5Web of Science - 5
Co-authors Andrew Boyle, Darryl Knight, Lucy Murtha
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 - 3Web of Science - 3
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 c... [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 associated 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
Citations Scopus - 3Web of Science - 2
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 m... [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 - 5Web of Science - 5
2015 Schuliga M, 'NF-kappaB Signaling in Chronic Inflammatory Airway Disease', BIOMOLECULES, 5 1266-1283 (2015)
DOI 10.3390/biom5031266
Citations Scopus - 71Web of Science - 77
2015 Schuliga M, 'The Inflammatory Actions of Coagulant and Fibrinolytic Proteases in Disease', MEDIATORS OF INFLAMMATION, (2015)
DOI 10.1155/2015/437695
Citations Scopus - 25Web of Science - 24
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)
DOI 10.1139/cjpp-2014-0391
Citations Scopus - 16Web of Science - 11
2014 Alkhouri H, Poppinga WJ, Tania NP, Ammit A, Schuliga M, 'Regulation of pulmonary inflammation by mesenchymal cells', Pulmonary Pharmacology and Therapeutics, 29 156e165-156e165 (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 - 15Web of Science - 18
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 [ 3H]-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 - 13Web of Science - 13
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 - 14
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 - 12
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 - 26Web of Science - 25
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 - 31Web of Science - 33
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 - 54Web of Science - 50
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 - 17Web of Science - 19
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 - 37Web of Science - 32
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)
DOI 10.1165/rcmb.2008-0361OC
Citations Scopus - 21Web of Science - 21
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 - 73Web of Science - 62
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 - 60
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 KCa3.1 in HASM cells and investigate its role in proliferation. Smooth muscle cells derived from human airways were grown in vitro and KCa3.1 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 KCa3.1 channel mRNA, protein, and activity with up-regulation evident after transforming growth factor-ß stimulation. Pharmacologic inhibition of KCa3.1 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 KCa3.1 channels in HASM cells. In addition, we have shown that KCa3.1 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 - 62
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 - 45Web of Science - 40
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 - 47Web of Science - 44
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 Sidor C, D'Amato R, Miller KD, 'The potential and suitability of 2-methoxyestradiol in cancer therapy', CLINICAL CANCER RESEARCH, 11 6094-6095 (2005)
DOI 10.1158/1078-0432.CCR-05-0724
Citations Scopus - 9Web of Science - 8
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
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 - 114Web of Science - 112
Show 31 more journal articles

Conference (40 outputs)

Year Citation Altmetrics Link
2018 Schuliga M, Waters D, Blokland K, Jaffar J, Westall G, Burgess J, et al., 'MITOCHONDRIAL DYSFUNCTION REINFORCES THE SENESCENT PHENOTYPE IN IPF LUNG FIBROBLASTS', RESPIROLOGY (2018)
Co-authors Darryl Knight, Christopher Grainge
2018 Blokland K, Waters D, Schuliga M, Grainge C, Mutsaers S, Prele C, et al., 'SENESCENT LUNG FIBROBLASTS ATTENUATE ALVEOLAR EPITHELIAL CELL PROLIFERATION AND MIGRATION IN IPF', RESPIROLOGY (2018)
Co-authors Darryl Knight, Christopher Grainge
2018 Waters D, Schuliga M, Blockland K, Burgess J, Grainge C, Westall G, et al., 'STAT3 ACTIVATION REINFORCES SENESCENCE IN HUMAN LUNG FIBROBLASTS', RESPIROLOGY (2018)
Co-authors Christopher Grainge, Darryl Knight
2017 Stewart AG, Li M, Langenbach S, Harris T, Keenan C, Jativa F, et al., 'Steroid-Enhancing Casein Kinase Inhibitors Have Anti-Fibrotic Efficacy', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
2017 Mitke A, Schuliga M, Harris T, Jativa F, Lee P, Jaffar J, et al., 'Soft Microenvironments Effectively Suppress Fibrogenesis Pathways In Control But Not In Idiopathic Pulmonary Fibrosis (ipf)-Derived Fibroblasts', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
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 Christopher Grainge, Darryl Knight
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 D, Waters DW, Fogarty E, Khalil N, Burgess JK, et al., 'Lung Fibroblasts Of Ipf Patients Display Senescence-Like Features In Vitro', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Christopher Grainge, Darryl Knight
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 Christopher Grainge, Darryl Knight
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, 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 (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.2012-0151OC
Citations Scopus - 23Web of Science - 23
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
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, St John, ANTIGUA & BARBU (2007)
DOI 10.1139/Y07-065
Citations Scopus - 16Web of Science - 14
Show 37 more conferences
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Grants and Funding

Summary

Number of grants 9
Total funding $1,233,200

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


20181 grants / $5,000

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

Funding body: Lung Foundation Australia

Funding body Lung Foundation Australia
Project Team Doctor Michael Schuliga, Professor Darryl Knight, Conjoint Associate Professor Christopher Grainge
Scheme Lizotte Family Research Award for Interstitial Pulmonary Fibrosis Research
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1801058
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

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: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Michael Schuliga, Conjoint Associate Professor Christopher Grainge, Professor Darryl Knight
Scheme Research Funding
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700697
Type Of Funding C3112 - Aust Not for profit
Category 3112
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
Current6

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2018 PhD Acute Exacerbation-Idiopathic Pulmonary Fibrosis (AE-IPF): The Role of Alveolar Epithelial Cell Senescence PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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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