Tissue Repair Unit
Many forms of lung disease can be regarded as the interaction between tissue injury and subsequent attempts to heal the affected tissues.
The Tissue Repair Group are committed to assessing the mechanisms regulating interactions between cells, the matrix surrounding cells and the different molecules released following injury. These interactions stimulate cells to respond in different ways, including by proliferation, migration, invasion, differentiation and collagen production. Diseases arising from abnormal tissue repair include asthma, pulmonary fibrosis, chronic obstructive lung disease (COPD), adhesions and cancer. The focus of their work is in two areas:
Firstly, the Group is examining how lung injury leads to the development of fibrosis (scar tissue in the lung). The cause of Idiopathic Pulmonary Fibrosis (IPF) is unknown but it is widely accepted that repeated injury to the epithelium leads to dysregulated healing, initiating a cascade of processes resulting in ﬁbroblast / myoﬁbroblast accumulation and overproduction and deposition of collagen.
Secondly, they are investigating the mechanisms underlying mesothelial healing, and the role of the mesothelial cell and mesothelial stem cell in normal repair; the formation of post-operative adhesions; and the factors that regulate the development and growth of malignant mesothelioma.
Current research projects
STAT3 regulation of cell responses in IPF
Epithelial-mesenchymal cell communication towards new therapeutic targets for fibrosis
Fibroblast Scenecence as a driver of pulmonary fibrosis
The Immune regulation of Idiopathic Pulmonary Fibrosis
Investigating the role of specific B cell subsets in chronic lung disease
miRNAs in mesothelioma
The hedgehog signalling pathway in mesothelioma
- PhD Candidate, Tylah Miles awarded the Australian Postgraduate Award Scholarship and the Lung Foundation Australia Bill van Nierop PhD Scholarship, 2018.
- Awarded NHMRC Project Grant for research into epithelial-mesenchymal cell communication; towards new therapeutic targets for fibrosis.
- Associate Professor Steve Mutsaers awarded the Alan King Westcare Grant 2017 for the effects of infection on mesothelial gene transcription: a role for immune check point regulation in chronic disease.
- Awarded the UHU Seed Funding Grant for investigating the role of specific B cell subsets in chronic lung disease.
- Awarded the UHU Collaborative Grant for Mesothelial cell involvement in serosal repair and adhesion formation.
- Celada LJ, Kropski JA, Herazo-Maya JD, Luo W, Creecy A, Abad AT, Chioma OS, Lee G, Hassell NE, Shaginurova GI, Wang Y, Johnson JE, Kerrigan A, Mason WR, Baughman RP, Ayers GD, Bernard GR, Culver DA, Montgomery CG, Maher TM, Molyneaux PL, Noth I, Mutsaers SE, Prele CM, Peebles RS Jr, Newcomb DC, Kaminski N, Blackwell TS, Van Kaer L, Drake WP. PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production. Sci Transl Med. 2018 Sep 26;10(460).
- Schuliga M, Pechkovsky DV, Read J, Waters DW, Blokland KEC, Reid AT, Hogaboam CM, Khalil N, Burgess JK, Prêle CM, Mutsaers SE, Jaffar J, Westall G, Grainge C, Knight DA. Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts. J Cell Mol Med. 2018 Dec;22(12):5847-5861. doi: 10.1111/jcmm.13855. Epub 2018 Sep 26.
- Hynds RE, Gowers KHC, Nigro E, Butler CR, Bonfanti P, Giangreco A, Prêle CM, Janes SM. Cross-talk between human airway epithelial cells and 3T3-J2 feeder cells involves partial activation of human MET by murine HGF. PLoS One. 2018 May 17;13(5):e0197129.
- Waters DW, Blokland KEC, Pathinayake PS, Burgess JK, Mutsaers SE, Prele CM, Schuliga M, Grainge CL, Knight DA. Fibroblast senescence in the pathology of idiopathic pulmonary fibrosis. Am J Physiol Lung Cell Mol Physiol. 2018 Aug 1;315(2):L162-L172. doi: 10.1152/ajplung.00037.2018. Epub 2018 Apr 26.
- Roman J, Mutsaers SE. Epigenetic Control of CXCL10: Regulating the Counterregulator in Idiopathic Pulmonary Fibrosis. Am J Respir Cell Mol Biol. 2018 Apr;58(4):419-420.