Dr  Tatt Jhong Haw

Dr Tatt Jhong Haw

Postdoctoral Research Fellow

School of Medicine and Public Health

Career Summary

Biography

Since 2015, Dr. Haw has published 15 manuscripts including 2 as first author, 12 as co-author and 1 editorial in high impact journals. In addition to these, he is also a corresponding author on a review published in 2015 (doi:10.9734/BMRJ/2015/13907). He has >15 conference publications at major Australia and international conferences. He has contributed immensely to the successful award of NMHRC grant (Prof Philip Hansbro, APP1137995; worth $925,000) in 2017. Dr. Haw was also a Finalist for the HMRI Health and Medical Research Project Grant 2018, recipient of TSANZ Boehringer Ingelheim COPD Research Award 2018 ($30,000) and University of Newcastle PRC of Healthy Lung Travel Award 2019 ($900).

Between 2016 to 2018, Dr. Haw worked as a research assistant and managed >12 industry projects with prominent Australian and international pharmaceutical research companies, namely Allakos, PharmAkea, AusBio, Pharmaxis and Genentech. He performed this role on a full-time basis (1.0 FTE). These projects revolved around investigating experimental/clinical therapeutics in animal models.

In 2019, Dr. Haw worked as a research assistant under A/Prof. Jay Horvat at HMRI. He assisted with research on respiratory health, namely asthma and lung aging. These projects centred around elucidating the complex and intricate molecular pathways that underpin the development/progression of respiratory diseases. He has extensive experience with in vivo and in vitro models of respiratory diseases (e.g. Influenza infection, asthma and smoking-induced lung diseases).

In June 2020, Dr. Haw took up a new position with Cardiometabolic, Cardio-oncology and Heart Failure research group at HMRI. With the support of A/Prof Doan Ngo and A/Prof Aaron Sverdlov, Dr. Haw will initially work as research assistant to acclimatise with the new group and build up his knowledge on the emerging and exciting field of cardio-oncology. Dr. Haw will restart his ECR career as a Postdoctoral Research Fellow at the start of 2021 and spearhead an exciting new cardio-oncology project that focus on investigating cardiotoxicity of anti-cancer agents in human inducible pluripotent stem cells-derived cardiac myocytes. The aim of the project is to identify new therapeutics to mitigate cardiotoxicity induced by current anti-cancer therapies.

Qualifications

  • Doctor of Philosophy, University of Newcastle
  • Bachelor of Science (Honours)(Biomedical), International Medical University - Malaysia

Keywords

  • Cardio-oncology
  • Human induced-pluripotent stem cells
  • Cardio-respiratory health
  • Cardiovascular disease
  • Cardioprotection
  • Industry project
  • Environmental determinants
  • Bushfire particulate
  • Drug discovery

Languages

  • English (Fluent)
  • Cantonese (Fluent)
  • Malay (Fluent)

Fields of Research

Code Description Percentage
320101 Cardiology (incl. cardiovascular diseases) 40
321199 Oncology and carcinogenesis not elsewhere classified 40
320103 Respiratory diseases 20

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Research Fellow University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
1/6/2020 - 31/12/2020 Research Assistant University of Newcastle
Faculty of Health and Medicine
18/8/2016 - 31/5/2020 Research Associate University of Newcastle
Faculty of Health and Medicine
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Publications

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


Journal article (19 outputs)

Year Citation Altmetrics Link
2022 Tu X, Kim RY, Brown AC, de Jong E, Jones-Freeman B, Ali MK, et al., 'Airway and parenchymal transcriptomics in a novel model of asthma and COPD overlap.', J Allergy Clin Immunol, (2022)
DOI 10.1016/j.jaci.2022.04.032
Co-authors Chantal Donovan, Jay Horvat, Philip Hansbro, Alexandra Brown, Darryl Knight, Malcolm Starkey, Peter Wark, Paul Foster, Henry Gomez
2021 Skerrett-Byrne DA, Bromfield EG, Murray HC, Jamaluddin MFB, Jarnicki AG, Fricker M, et al., 'Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease', Respirology, 26 960-973 (2021) [C1]

Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with n... [more]

Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with none able to reverse disease or stop its progression. We explored the major molecular changes in COPD pathogenesis. Methods: We employed quantitative label-based proteomics to map the changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that is induced over 8 weeks and progresses over 12 weeks. Results: Quantification of 7324 proteins enabled the tracking of changes to the proteome. Alterations in protein expression profiles occurred in the induction phase, with 18 and 16 protein changes at 4- and 6-week time points, compared to age-matched controls, respectively. Strikingly, 269 proteins had altered expression after 8 weeks when the hallmark pathological features of human COPD emerge, but this dropped to 27 changes at 12 weeks with disease progression. Differentially expressed proteins were validated using other mouse and human COPD bronchial biopsy samples. Major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] and RNA-binding protein Musashi homologue 2 [MSI2]) and modulators of inflammatory responses (S100A1) were notable. Mitochondrial dysfunction and changes in oxidative stress proteins also occurred. Conclusion: We provide a detailed proteomic profile, identifying proteins associated with the pathogenesis and disease progression of COPD establishing a platform to develop effective new treatment strategies.

DOI 10.1111/resp.14111
Citations Scopus - 7Web of Science - 7
Co-authors Michael Fricker, Peter Wark, Rodney Scott, Philip Hansbro, Elizabeth Bromfield, Matt Dun, Muhammad Jamaluddin, Heather Murray, David Skerrett-Byrne, Brett Nixon
2021 Kim RY, Sunkara KP, Bracke KR, Jarnicki AG, Donovan C, Hsu AC, et al., 'microRNA-21-mediated SATB1/S100A9/NF-kappa B axis promotes chronic obstructive pulmonary disease pathogenesis', SCIENCE TRANSLATIONAL MEDICINE, 13 (2021) [C1]
DOI 10.1126/scitranslmed.aav7223
Citations Scopus - 4Web of Science - 4
Co-authors Philip Hansbro, Jay Horvat, Chantal Donovan, Emma Beckett, Paul Foster, Alan Hsu, Peter Wark
2021 Chen D, Kelly C, Haw TJ, Lombard JM, Nordman IIC, Croft AJ, et al., 'Heart Failure in Breast Cancer Survivors: Focus on Early Detection and Novel Biomarkers', Current Heart Failure Reports, 18 362-377 (2021)

Purpose of Review: Breast cancer survival rate has greatly improved in the last two decades due to the emergence of next-generation anti-cancer agents. However, cardiotoxicity rem... [more]

Purpose of Review: Breast cancer survival rate has greatly improved in the last two decades due to the emergence of next-generation anti-cancer agents. However, cardiotoxicity remains a significant adverse effect arising from traditional and emerging chemotherapies as well as targeted therapies for breast cancer patients. In this review, we will discuss cardiotoxicities of both traditional and emerging therapies for breast cancer. We will discuss current practices to detect cardiotoxicity of these therapies with the focus on new and emerging biomarkers. We will then focus on ¿omics approaches, especially the use of epigenetics to discover novel biomarkers and therapeutics to mitigate cardiotoxicity. Recent Findings: Significant cardiotoxicities of conventional chemotherapies remain and new and unpredictable new forms of cardiac and/or vascular toxicity emerge with the surge in novel and targeted therapies. Yet, there is no clear guidance on detection of cardiotoxicity, except for significant left ventricular systolic dysfunction, and even then, there is no uniform definition of what constitutes cardiotoxicity. The gold standard for detection of cardiotoxicity involves a serial echocardiography in conjunction with blood-based biomarkers to detect early subclinical cardiac dysfunction. However, the ability of these tests to detect early disease remains limited and not all forms of toxicity are detectable with these modalities. Summary: There is an unprecedented need to discover novel biomarkers that are sensitive and specific for early detection of subclinical cardiotoxicity. In that space, novel echocardiographic techniques, such as strain, are becoming more common-place and new biomarkers, discovered by epigenetic approaches, seem to become promising alternatives or adjuncts to conventional non-specific cardiac biomarkers.

DOI 10.1007/s11897-021-00535-w
Citations Scopus - 1
Co-authors Doan Ngo, Aaron Sverdlov
2020 Schanin J, Gebremeskel S, Korver W, Falahati R, Butuci M, Haw TJ, et al., 'A monoclonal antibody to Siglec-8 suppresses non-allergic airway inflammation and inhibits IgE-independent mast cell activation', MUCOSAL IMMUNOLOGY, 14 366-376 (2020) [C1]
DOI 10.1038/s41385-020-00336-9
Citations Scopus - 26Web of Science - 24
Co-authors Philip Hansbro
2019 Donovan C, Starkey MR, Kim RY, Rana BMJ, Barlow JL, Jones B, et al., 'Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease', Journal of Leukocyte Biology, 105 143-150 (2019) [C1]

Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogen... [more]

Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1 -/- and Rora fl/fl Il7r Cre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1 -/- , and Rora fl/fl Il7r Cre mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12¿weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 -/- , and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 -/- normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora fl/fl Il7r Cre mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.

DOI 10.1002/JLB.3AB0518-178R
Citations Scopus - 31Web of Science - 31
Co-authors Chantal Donovan, Jay Horvat, Philip Hansbro, Peter Wark, Malcolm Starkey, Kurtis Budden, Paul Foster
2019 Liu G, Cooley MA, Jarnicki AG, Borghuis T, Nair PM, Tjin G, et al., 'Fibulin-1c regulates transforming growth factor-beta activation in pulmonary tissue fibrosis', JCI INSIGHT, 4 (2019) [C1]
DOI 10.1172/jci.insight.124529
Citations Scopus - 27Web of Science - 28
Co-authors Darryl Knight, Jay Horvat, Philip Hansbro, Alan Hsu, Peter Wark, Michael Fricker
2019 Nair PM, Starkey MR, Haw TJ, Liu G, Collison AM, Mattes J, et al., 'Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease', CLINICAL & TRANSLATIONAL IMMUNOLOGY, 8 (2019) [C1]
DOI 10.1002/cti2.1084
Citations Scopus - 8Web of Science - 6
Co-authors Joerg Mattes, Malcolm Starkey, Peter Wark, Nikki Verrills, Philip Hansbro, Adam Collison
2019 Starkey MR, Plank MW, Casolari P, Papi A, Pavlidis S, Guo Y, et al., 'IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis', EUROPEAN RESPIRATORY JOURNAL, 54 (2019) [C1]
DOI 10.1183/13993003.00174-2018
Citations Scopus - 31Web of Science - 26
Co-authors Philip Hansbro, Jay Horvat, Gerard Kaiko, Chantal Donovan, Paul Foster, Malcolm Starkey, Peter Wark
2018 Nair PM, Starkey MR, Haw TJ, Ruscher R, Liu G, Maradana MR, et al., 'RelB-deficient Dendritic Cells Promote the Development of Spontaneous Allergic Airway Inflammation.', American journal of respiratory cell and molecular biology, (2018) [C1]
DOI 10.1165/rcmb.2017-0242oc
Citations Scopus - 9Web of Science - 9
Co-authors Malcolm Starkey, Philip Hansbro
2018 Haw TJ, Starkey MR, Pavlidis S, Fricker M, Arthurs AL, Nair PM, et al., 'Toll-like receptor 2 and 4 have opposing roles in the pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease.', American journal of physiology. Lung cellular and molecular physiology, 314 L298-L317 (2018) [C1]
DOI 10.1152/ajplung.00154.2017
Citations Scopus - 35Web of Science - 33
Co-authors Philip Hansbro, Paul Foster, Jay Horvat, Michael Fricker, Malcolm Starkey
2017 Hansbro PM, Haw TJ, Starkey MR, Miyake K, 'Toll-like receptors in COPD', EUROPEAN RESPIRATORY JOURNAL, 49 (2017) [C1]
DOI 10.1183/13993003.00739-2017
Citations Scopus - 8Web of Science - 9
Co-authors Malcolm Starkey, Philip Hansbro
2017 Nair PM, Starkey MR, Haw TJ, Liu G, Horvat JC, Morris JC, et al., 'Targeting PP2A and proteasome activity ameliorates features of allergic airway disease in mice', Allergy: European Journal of Allergy and Clinical Immunology, 72 1891-1903 (2017) [C1]

Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase ... [more]

Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase with anti-inflammatory activity. The ubiquitin proteasome system (UPS) controls many cellular processes, including the initiation of inflammatory responses by protein degradation. We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL (S) ), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD. Methods: Acute AAD was induced in C57BL/6 mice by intraperitoneal sensitization with ovalbumin (OVA) in combination with intranasal (i.n) exposure to OVA. Chronic AAD was induced in mice with prolonged i.n exposure to crude house dust mite (HDM) extract. Mice were treated with vehicle, FTY720, AAL (S) , BORT or AAL (S) +BORT and hallmark features of AAD assessed. Results: AAL (S) reduced the severity of acute AAD by suppressing tissue eosinophils and inflammation, mucus-secreting cell (MSC) numbers, type 2-associated cytokines (interleukin (IL)-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-responsiveness (AHR). FTY720 only suppressed tissue inflammation and IgE. BORT reduced bronchoalveolar lavage fluid (BALF) and tissue eosinophils and inflammation, IL-5, IL-13 and AHR. Combined treatment with AAL (S) +BORT had complementary effects and suppressed BALF and tissue eosinophils and inflammation, MSC numbers, reduced the production of type 2 cytokines and AHR. AAL (S) , BORT and AAL (S) +BORT also reduced airway remodelling in chronic AAD. Conclusion: These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.

DOI 10.1111/all.13212
Citations Scopus - 15Web of Science - 16
Co-authors Jay Horvat, Nikki Verrills, Malcolm Starkey, Philip Hansbro
2017 Kim RY, Horvat JC, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase mediated suppression of histone deacetylase 2', Journal of Allergy and Clinical Immunology, 139 519-532 (2017) [C1]

Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of und... [more]

Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of understanding of the mechanisms of disease pathogenesis. Steroid-insensitive asthma is associated with respiratory tract infections and noneosinophilic endotypes, including neutrophilic forms of disease. However, steroid-insensitive patients with eosinophil-enriched inflammation have also been described. The¿mechanisms that underpin infection-induced, severe steroid-insensitive asthma can be elucidated by using mouse models of disease. Objective We sought to develop representative mouse models of severe, steroid-insensitive asthma and to use them to identify pathogenic mechanisms and investigate new treatment approaches. Methods Novel mouse models of Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory¿tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21¿specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion We identify a previously unrecognized role for an¿miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.

DOI 10.1016/j.jaci.2016.04.038
Citations Scopus - 128Web of Science - 131
Co-authors Paul Foster, Joerg Mattes, Jemma Mayall, Jay Horvat, Malcolm Starkey, Philip Hansbro, Simon Keely
2017 Liu G, Cooley MA, Nair PM, Donovan C, Hsu AC, Jarnicki AG, et al., 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c', JOURNAL OF PATHOLOGY, 243 510-523 (2017) [C1]
DOI 10.1002/path.4979
Citations Scopus - 61Web of Science - 61
Co-authors Alexandra Brown, Peter Wark, Alan Hsu, Christopher Grainge, Philip Hansbro, Jay Horvat, Hock Tay, Darryl Knight, Chantal Donovan, Paul Foster
2017 Hsu AC-Y, Dua K, Starkey MR, Haw T-J, Nair PM, Nichol K, et al., 'MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD', JCI INSIGHT, 2 (2017) [C1]
DOI 10.1172/jci.insight.90443
Citations Scopus - 74Web of Science - 66
Co-authors Paul Foster, Katherine Baines, Malcolm Starkey, Peter Wark, Alan Hsu, Philip Hansbro
2016 Haw TJ, Starkey MR, Nair PM, Pavlidis S, Liu G, Nguyen DH, et al., 'A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease', Mucosal Immunology, 9 859-872 (2016) [C1]

Chronic obstructive pulmonary disease (COPD) is a life-Threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective ... [more]

Chronic obstructive pulmonary disease (COPD) is a life-Threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-Type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL + CD11b + monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.

DOI 10.1038/mi.2015.111
Citations Scopus - 45Web of Science - 44
Co-authors Alan Hsu, Philip Hansbro, Malcolm Starkey, Jay Horvat, Darryl Knight, Peter Wark, Paul Foster, Joerg Mattes, Adam Collison
2016 Gang L, Hsu A, Cooley MA, Jarnicki AG, Nair PM, Haw TJ, et al., 'Fibulin-1 regulates the pathogenesis of tissue remodeling in respiratory diseases', Journal of Clinical Investigation Insight, 1 (2016) [C1]
DOI 10.1172/jci.insight.86380
Citations Web of Science - 70
Co-authors Michael Fricker, Alan Hsu, Philip Hansbro, Jay Horvat, Darryl Knight, Marjorie Walker, Peter Wark
2015 Hsu ACY, Starkey MR, Hanish I, Parsons K, Haw TJ, Howland LJ, et al., 'Targeting PI3K-p110a suppresses influenza virus infection in chronic obstructive pulmonary disease', American Journal of Respiratory and Critical Care Medicine, 191 1012-1023 (2015) [C1]

Rationale: Chronic obstructive pulmonary disease (COPD) and influenza virus infections are major global health issues. Patients with COPD are more susceptible to infection, which ... [more]

Rationale: Chronic obstructive pulmonary disease (COPD) and influenza virus infections are major global health issues. Patients with COPD are more susceptible to infection, which exacerbates their condition and increases morbidity and mortality. The mechanisms of increased susceptibility remain poorly understood, and current preventions and treatments have substantial limitations. Objectives: To characterize the mechanisms of increased susceptibility to influenza virus infection in COPD and the potential for therapeutic targeting. Methods: We used a combination of primary bronchial epithelial cells (pBECs) from COPD and healthy control subjects, a mouse model of cigarette smoke-induced experimental COPD, and influenza infection. The role of the phosphoinositide-3-kinase (PI3K) pathway was characterized using molecular methods, and its potential for targeting assessed using inhibitors. Measurements and Main Results: COPDpBECs were susceptible to increased viral entry and replication. Infected mice with experimental COPD also had more severe infection (increased viral titer and pulmonary inflammation, and compromised lung function). These processes were associated with impaired antiviral immunity, reduced retinoic acid-inducible gene-I, and IFN/cytokine and chemokine responses. Increased PI3K-p110a levels and activity inCOPDpBECs and/or mice were responsible for increased infection and reduced antiviral responses. Global PI3K, specific therapeutic p110a inhibitors, or exogenous IFN-b restored protective antiviral responses, suppressed infection, and improved lung function. Conclusions: The increased susceptibility of individuals with COPD to influenza likely results from impaired antiviral responses, which are mediated by increased PI3K-p110a activity. This pathway may be targeted therapeutically in COPD, or in healthy individuals, during seasonal or pandemic outbreaks to prevent and/or treat influenza.

DOI 10.1164/rccm.201501-0188OC
Citations Scopus - 97Web of Science - 94
Co-authors Paul Foster, Alan Hsu, Philip Hansbro, Malcolm Starkey, Peter Wark, Darryl Knight
Show 16 more journal articles

Conference (15 outputs)

Year Citation Altmetrics Link
2022 Gomez H, Ilic D, Robinson P, Zosky G, Haw JT, Vanka K, et al., 'Assessing the respiratory and cardiovascular effects of landscape fire smoke', RESPIROLOGY (2022)
Co-authors Thava Palanisami, Vanessa Mcdonald, Dusan Ilic, Jay Horvat, Tesfalidet Beyene, Vanessa Murphy
2020 Hansbro NG, Pacitti D, Brown A, Torregrossa R, Balachandran L, Kumar V, et al., 'Mitochondria-targeted Sulfide Delivery Molecules - New and Novel Players that can Suppress and Reverse Cigarette Smoke-induced Inflammasome Activity', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2020)
Co-authors Philip Hansbro
2020 Whiteman M, Pacitti D, Brown A, Torregrossa R, Balachandran L, Kumar V, et al., 'Suppression and Reversal of Cigarette Smoke-Induced Inflammasome Activation/Activity and Lung Injury by Novel Mitochondria-Targeted Sulfide Delivery Molecules', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, ELECTR NETWORK (2020)
Co-authors Philip Hansbro
2020 Gomez H, Vanders R, Donovan C, Haw JT, Budden K, Balachandran L, et al., 'MATERNAL CIGARETTE SMOKE-EXPOSURE AFFECTS SUSCEPTIBILITY TO RESPIRATORY VIRAL INFECTION IN OFFSPRING', RESPIROLOGY (2020)
Co-authors Kurtis Budden, Jay Horvat, Philip Hansbro, Chantal Donovan
2017 Starkey MR, Dua K, Hsu AC, Nair PM, Haw TJ, Nguyen DH, et al., 'Interleukin-13 Predisposes To More Severe Influenza Infection In Mice And Human Epithelial Cells By Suppressing Interferon Responses And Activating The Microrna-21/pi3k Signaling Pathway', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Citations Web of Science - 1
Co-authors Malcolm Starkey, Alan Hsu, Jay Horvat, Philip Hansbro, Peter Wark
2017 Starkey MR, Nguyen DH, Kim RY, Nair PM, Haw TJ, Horvat JC, et al., 'Early Life Respiratory Bacterial Infection-Induced Chronic Lung Disease Is Driven By A Novel Tlr2/il-13/mir-21/pi3k Signaling Pathway', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Washington, DC (2017)
Co-authors Jay Horvat, Malcolm Starkey, Philip Hansbro
2017 Liu G, Cooley MA, Jarnicki AG, Hsu AC-Y, Nair PM, Haw TJ, et al., 'FIUBLIN-1C PLAYS CRITICAL ROLES IN LUNG REMODELLING IN IDIOPATHIC PULMONARY FIBROSIS', RESPIROLOGY (2017)
Co-authors Michael Fricker, Alan Hsu, Philip Hansbro, Jay Horvat, Darryl Knight, Marjorie Walker
2017 Kim R, Sunkara K, Jarnicki A, Bracke K, Haw TJ, Wark P, et al., 'MicroRNA-21 DRIVES EXPERIMENTAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE THROUGH A SATB1/S100A9/NF-kappa B AXIS', RESPIROLOGY (2017)
Co-authors Paul Foster, Philip Hansbro, Jay Horvat, Peter Wark
2016 Horvat J, Kim R, Pinkerton J, Rae B, Starkey M, Essilfie A-T, et al., 'Identification of therapeutic targets for steroid-insensitive asthma using models that represent different clinical subtypes of disease', EUROPEAN RESPIRATORY JOURNAL (2016)
DOI 10.1183/13993003.congress-2016.PA563
Co-authors Jay Horvat, Simon Keely, Paul Foster, Philip Hansbro, Joerg Mattes
2016 Starkey MR, Dua K, Hsu AC, Nair PM, Haw TJ, Nguyen DH, et al., 'Interleukin-13 predisposes to more severe influenza infection in mice and human epithelial cells by suppressing interferon responses and activating the microRNA-21/PI3K signaling pathway', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Paul Foster, Alan Hsu, Philip Hansbro, Malcolm Starkey, Peter Wark, Jay Horvat
2016 Starkey MR, Nguyen DH, Kim RY, Haw TJ, Nair PM, Essilfie AT, et al., 'Early-life respiratory bacterial infection-induced chronic lung disease is driven by a novel TLR2/IL-13/miR-21/PI3K signaling pathway', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Paul Foster, Philip Hansbro, Malcolm Starkey, Jay Horvat
2015 Kim R, Horvat J, Pinkerton J, Starkey M, Essilfie A, Mayall J, et al., 'INFECTION-INDUCED MICRORNA-21 DRIVES SEVERE, STEROID-INSENSITIVE EXPERIMENTAL ASTHMA BY AMPLIFYING PI3K-MEDIATED SUPPRESSION OF HDAC2', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
Co-authors Joerg Mattes, Paul Foster, Simon Keely, Philip Hansbro, Malcolm Starkey, Jay Horvat, Jemma Mayall
2015 Hansbro P, Haw T, Nair P, Hanish I, Nguyen D, Liu G, et al., 'Tumour necrosis factor-related apoptosis inducing ligand promotes the development of experimental chronic obstructive pulmonary disease', JOURNAL OF IMMUNOLOGY, New Orleans, LA (2015)
Co-authors Joerg Mattes, Philip Hansbro, Adam Collison, Jay Horvat, Darryl Knight
2015 Hansbro PM, Kim RY, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'Infection-Induced Microrna-21 Drives Severe, Steroid-Insensitive Experimental Asthma By Amplifying PhosphoINOSitide-3-Kinase (pi3k)-Mediated Suppression Of Histone Deacetylase (hdac)2', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Denver, CO (2015)
Co-authors Joerg Mattes, Paul Foster, Simon Keely, Philip Hansbro, Malcolm Starkey, Jay Horvat
2014 Starkey M, Hanish I, Dua K, Nair P, Haw T, Hsu A, et al., 'Interleukin-13 predisposes mice to more severe influenza infection by suppressing interferon responses and activating microRNA-21/PI3K', CYTOKINE, Melbourne, AUSTRALIA (2014) [E3]
DOI 10.1016/j.cyto.2014.07.182
Citations Web of Science - 3
Co-authors Peter Wark, Darryl Knight, Jay Horvat, Philip Hansbro, Alan Hsu, Paul Foster, Malcolm Starkey
Show 12 more conferences
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Grants and Funding

Summary

Number of grants 4
Total funding $128,182

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


20221 grants / $75,000

Investigating the cardiopulmonary impacts of prolonged exposure to bushfire smoke particulate matter and other environmental hazards in Regional Australia$75,000

Funding body: National Heart Foundation of Australia

Funding body National Heart Foundation of Australia
Project Team Doctor Tatt Jhong Haw, Doctor Henry Gomez, Associate Professor Jay Horvat, Associate Professor Doan Ngo
Scheme Vanguard Grant
Role Lead
Funding Start 2022
Funding Finish 2022
GNo G2100499
Type Of Funding C1700 - Aust Competitive - Other
Category 1700
UON Y

20212 grants / $23,182

Discovering and developing novel cardioprotective therapies to mitigate cardiovascular complications of cancer therapies. $18,182

Funding body: Hunter New England Local Health District

Funding body Hunter New England Local Health District
Project Team Doctor Tatt Jhong Haw, Associate Professor Doan Ngo, Dr Maria Aslam, Dr Rohan Bhagwandeen
Scheme John Hunter Hospital Charitable Trust Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo G2100266
Type Of Funding C2400 – Aust StateTerritoryLocal – Other
Category 2400
UON Y

Discovering and developing novel cardioprotective therapies to mitigate cardiovascular complications of cancer therapies$5,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Tatt Jhong Haw
Scheme Research Grant
Role Lead
Funding Start 2021
Funding Finish 2021
GNo G2100180
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

20191 grants / $30,000

Targeting cellular senescence as a novel therapeutic in Chronic Obstructive Pulmonary Disease$30,000

Funding body: Thoracic Society of Australia and New Zealand

Funding body Thoracic Society of Australia and New Zealand
Project Team Doctor Tatt Jhong Haw, Professor Philip Hansbro, Associate Professor Jay Horvat
Scheme TSANZ Boehringer Ingelheim COPD Research Award
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1900722
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y
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Research Supervision

Number of supervisions

Completed1
Current0

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2019 Honours Investigating the role of TLR2 and TLR4 in host-microbiome interactions in experimental COPD Microbiology, College of Health, Medicine & Wellbeing - The University of Newcastle Principal Supervisor
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Research Projects

Discovering and developing novel cardioprotective therapies to mitigate cardiovascular complications of cancer therapies 2020 -

Cancer survival rate has greatly improved in the last two decades due to the emergence of next-generation anti-cancer agents. However, some anti-cancer treatments unexpectedly caused cardiotoxicity and led to cardiovascular complications (e.g. heart failure). This has led to early disruption or discontinuation of potentially life-saving anti-cancer therapy that can be detrimental to patients’ health, quality of life and survival. Therefore, there is an urgent need to identify novel cardioprotective therapies to mitigate cardiotoxicity whilst preserving the effectiveness of current anti-cancer therapies.

We propose an exciting pilot study to identify novel cardioprotective drugs from of a library of preclinical/clinical drugs by high-throughput screening. We may identify drugs with previously unrecognised beneficial cardioprotective effects and repurpose them into novel therapies to mitigate cardiotoxicity. The outcome of this project may revolutionise healthcare policies, allow health practitioners to make better informed decision to reduce risk of cardiotoxicity and improve outcomes/survival in cancer patients.


Human Inducible Pluripotent Stem Cells 2021 -


Investigating the cardiopulmonary impacts of prolonged exposure to bushfire smoke particulate matter and other environmental hazards in Regional Australia 2022 -

Particulate matters from urbanisation, industry pollution, and natural disasters (e.g., bushfire) can aggravate cardiopulmonary health and lead to hospitalisation or death. There is no ‘safe’ lower exposure levels and adverse cardiopulmonary events can occur at levels below current regulatory standards. Thus, the impact of the catastrophic 2019/2020 Black Summer bushfires on cardiopulmonary health is unprecedented. Approximately 10 million Australians were exposed to bushfire smoke for several months. The impact of bushfire smoke exposure on cardiopulmonary health remains largely unknown. Our preliminary findings suggest that prolonged exposure to bushfire smoke is detrimental to cardiopulmonary health. To address this clinical urgency, we propose a multidisciplinary and collaborative investigation involving from cardiovascular and respiratory researchers. We will use a combination of a highly representative animal model and human cardiac cell studies to comprehensively assess the impacts of bushfire smoke exposure on cardiopulmonary health. 


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News

Funding awarded to fight Australia’s single biggest killer

October 20, 2021

Six University of Newcastle researchers have secured more than $1million in Heart Foundation funding to research the causes, prevention, and treatment of heart disease, stroke and related conditions.

Dr Tatt Jhong Haw

Position

Postdoctoral Research Fellow
Cardiometabolic Research Group
School of Medicine and Public Health
College of Health, Medicine and Wellbeing

Contact Details

Email tattjhong.haw@newcastle.edu.au
Phone 0240420193
Link Twitter

Office

Room HMRI/Level 3 East Wing
Building HMRI
Location New Lambton Heights

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