George Bou-Gharios PhD
John Baugh PhD
John Robert Couchman Ph.D
Adam J. Engler PhD
Karen English PhD
Peter Friedl MD, PhD
Garry Duffy PhD
Caitriona Lally PhD
Tanya Levingstone PhD
Charles D. Little PhD
Aideen Ryan PhD
Liliana Schaefer MD, PhD
Charles Streuli MA, PhD
George Bou-Gharios PhD
George Bou-Gharios is a Professor of Matrix Biology at the University of Liverpool. His group is particularly interested in the transcriptional regulation of matrix molecules that maintain connective tissue homeostasis. Investigating key enhancer sequences that regulate embryonic and adult matrix expression, in a cell-specific manner, enabling them to use pre-clinical models to study genetic gain and loss of function revealing the mechanism(s) that underlie some of the major connective tissue pathologies.
John Baugh PhD
The Baugh research group is interested in the mechanisms involved in the onset and progression of aberrant tissue remodelling in inflammatory lung diseases. In particular, they are trying to elucidate the mechanisms that control fibroblast activation, proliferation and differentiation in patients with idiopathic pulmonary fibrosis (IPF).
Disease progression in IPF is associated with alveolar epithelial damage followed by the development of areas of fibroblast proliferation and differentiation. Tissue damage leads to increased matrix deposition, and ultimately severe derangement of gas exchange units. Loss of alveolar function leads to impaired ventilation, decreased lung function and both systemic and local tissue hypoxia.
There are two main projects related to inflammatory gene expression in the lung. The first is focused upon understanding the transcriptional regulation of the macrophage migration inhibitory factor (MIF) gene. They recently described a functional tetranucleotide-repeat element in the MIF promoter that correlates with disease severity in inflammatory disease such as rheumatoid arthritis, and are seeking to elucidate the mechanism by which this polymorphism affects gene expression.
Extending from these studies on the regulation of MIF expression the second main project is based upon the effects of hypoxia on pro-inflammatory gene expression in primary human lung fibroblasts derived from patients with various respiratory pathologies. The lungs are exquisitely sensitive to changes in atmospheric and blood oxygen levels and normally respond in order to maintain health of the organism. In some inflammatory lung diseases, however, it is believed that abnormal responses to hypoxia may contribute to exacerbated inflammation and aberrant tissue remodelling. The Baugh Lab are particularly interested in elucidating mechanisms by which hypoxia may drive aberrant remodelling in diseases such as IPF.
John Robert Couchman PhD
John Robert Couchman is Foundation Professor, Department of Biomedical Sciences and
Biotech Research & Innovation Centre (BRIC) University of
Copenhagen. His research areas include: Cell adhesion to
extracellular matrix, signalling from adhesion receptors, potential
involvement of cell surface proteoglycans and their ligands in
tumour progression, heparan sulphate biosynthesis and
regulation. Dr. Couchman has authored 168 publications in peer
review journals and is the current Editor-in-Chief of the Journal
of Histochemistry & Cytochemistry and Editorial Board member of the Journal of Biological
Chemistry. His research is focused in extracellular biology and the regulation of cell behaviour. Nearly all cells and tissues are in contact with, and adherent to, an extracellular matrix (ECM). Essential in all multicellular animals, ECM is required through development and for immune function, homeostasis, physical support and tissue repair. ECM takes many forms depending on its role, ranging from the connective tissues of skin and other organs, to skeletal structures that comprise cartilage and bone.
One important receptor that his lab focuses on is syndecan-4, a small heparan sulphate containing proteoglycan. We have established that it works in conjunction with integrin receptors to promote junctions known as focal adhesions.
Adam J. Engler is an Associate Professor of Bioengineering at UC San Diego, where he has been on the faculty since 2008. He also is a resident scientist at the Sanford Consortium for Regenerative Medicine. Dr. Engler previously trained with Drs. Dennis Discher at the University of Pennsylvania and Jean Schwarzbauer at Princeton University. His current research focuses on how physical and chemical properties of the niche regulates and misregulates cell function during disease and aging, with particular applications to heart disease and cancer. His lab makes natural and synthetic extracellular matrices with unique spatiotemporal properties to mimic niche conditions to improve cell behavior and commitment in vitro. His lab also studies these processes in vivo with aging model systems including Drosophila, rats, and rhesus monkeys. With over 75 papers and 16,000 citation, Dr. Engler’s work has been internationally recognized for it impact, including the 2008 Rupert Timpl Award from ISMB, the 2008 Rita Schaeffer Award from BMES, a 2009 NIH New Innovator Award, and the 2015 Y.C. Fung Award from ASME. Dr. Engler was the inaugural recipient of the Renato Iozzo Award from ASMB in 2014.
Karen English, PhD
Dr English leads the Cellular Immunology Laboratory in the Institute of Immunology at Maynooth University. The major focus of our research is the translation of cellular therapy for the treatment of inflammatory diseases. Mesenchymal stromal cells (MSC) are adult cells found in many tissues including bone marrow, adipose tissue and umbilical cord. MSC have potent anti-inflammatory and pro-reparative properties and for this reason are being tested as a cellular therapy for inflammatory disorders. The mechanisms of action used by MSC in protecting against inflammation and promoting repair and not well understood. To address this question, my lab utilises state of the art humanised mouse models of inflammatory disease including graft versus host disease and lung inflammation and fibrotic associated diseases. The overall goal of my research is to further understand how these cells mediate these positive effects and identify their interactions with cells of the immune system to optimise MSC therapy for the treatment of inflammatory disorders.
Peter Friedl holds the chair for Microscopical Imaging of the Cell at the NCMLS since October 2007, which includes the Core Facility for Microscopy at the Radboud University Nijmegen Medical Center. In addition, he fulfills the role of the head of the Cell Dynamics Laboratory and, since 11/2011 has a joint-appointment joint-faculty position as head of the imaging section at the David H. Koch Center, Department of Genitoureteal Oncology, MD Anderson Cancer Center, Houston, TX, USA. His research interest is the visualization of cell-matrix interactions and dynamic cell patterning during immune cell interactions and tumor invasion. Hi group therefore, use 3D extracellular matrix (ECM) based cell culture models and advanced imaging procedures, and more recently, the group has moved into in vivo-imaging of tumor and immune cell migration by multiphoton microscopy. This complements in vitro culture technology. These approaches have provided insight into the serial dynamics of T cell scanning across antigen-presenting cells and the diversity of tumor invasion mechanisms, as well as novel escape responses in tumor cell migration.
Garry Duffy, PhD
Dr Garry Duffy is Personal Professor of Anatomy, within the School of Medicine at the National University of Ireland Galway (NUIG) and Honorary Professor of Regenerative Medicine in the Tissue Engineering Research Group (TERG) at the Royal College of Surgeons in Ireland (RCSI). Garry is an expert in stem cell therapeutics and advanced biomaterials. He leads the Duffy Lab at NUIG, which is focused on developing advanced biomaterials to facilitate targeted delivery and future clinical translation of cell based therapeutics to treat chronic diseases. Central to this are the two European Consortia that Garry Coordinates, AMCARE and DRIVE, which gather a combined 18 industry, academic and clinical partners to design smart living biomaterial implants to treat myocardial infarction and diabetes, respectively.
Caitriona Lally, PhD
Prof. Caitríona Lally is a Professor in Bioengineering within the Department of Mechanical and Manufacturing Engineering and Principal Investigator in the Trinity Centre for Bioengineering (TCBE) in Trinity College Dublin (TCD). She received her BEng (Mechanical Engineering) and MEng (Biomedical Engineering) degrees from University of Limerick and in 2004 she obtained a PhD from Trinity College Dublin in the area of arterial biomechanics and cardiovascular stenting. Immediately following her Ph.D., she took up a lecturing position in the School of Mechanical & Manufacturing Engineering at Dublin City University, and was appointed senior lecturer in 2014. She recently returned to TCD in 2015 as a Professor in Bioengineering.
Prof. Lally leads a multidisciplinary research group focused on arterial tissue mechanics, vascular imaging, vascular mechanobiology and tissue engineering. Her goal is to gain critical insights into the role of mechanics in cardiovascular diseases, with particular focus on load induced remodelling and regeneration of arterial tissues at the material and cell level. She aims to develop novel diagnostic techniques for early detection of vascular degeneration and intravascular medical devices for the treatment of existing vascular disease.
Tanya Levingstone, PhD
Dr. Tanya Levingstone is an Assistant Professor in the School of Mechanical and Manufacturing Engineering in Dublin City University and an Honorary Lecturer in the Department of Anatomy in the Royal College of Surgeons in Ireland. Her research work focuses on the development of novel biomaterial based approaches for cartilage, bone and osteeochondral tissue engineering. Her work has a translational focus and has led to the 'bench to bedside' translation of a novel scaffold for osteochondral defect repair. In particular her research focuses on the investigation of the affects of mechanical properties and macromolecule incorporation on the direction of stem cell differentiation down osteogenic or chondrogenic routes. She also has ongoing research in the area of heart valve tissue engineering and in the development of novel materials for wound repair.
Charles D. Little is Professor at the Department of Anatomy and Cell Biology at the University of Kansas, USA. His laboratory aims to underline the importance of emergent biophysical patterns during formation of tissues and organs. Tissue and organ formation is largely an emergent process and the Little Lab aims to decipher the “missing” information residing in complex biomechanical code.
His Group investigate emergent mechanisms that rely on: 1) tissue-scale motion, 2) modulation of the biomechanical (material) properties of embryonic tissues, and 3) subsequent morphogenetic bending and folding based on the aforesaid tissue material properties. In other words, the critical morphogenetic displacements and folding events — which characterize all amniotes embryos — are manifested at the tissue scale (> 0.1mm) and are emergent, not hard-wired.
Towards this goal, experimental perturbations, time-lapse imaging and computational approaches aim to examine live quail embryos and de novo tissue and organ morphogenesis using multi-color fluorescence microscopy — one channel(s) for cell markers and the other channel(s) for extracellular matrix (ECM) fibers. In early bird embryos his group find little difference between the movements of individual cells versus the adjacent ECM, concluding that in amniote embryos a complex emergent biomechanical code largely governs early tissue formation and organogenesis.
Liliana Schaefer, M.D. is a Professor of Pharmacology at Goethe University, Frankfurt/Main, Germany. Following training in Internal Medicine/Nephrology at the University of Poznan, School of Medicine, Poland, she pursued graduate studies and obtained a Medical Doctor Degree from the University of Wuerzburg, Germany. After a postdoctoral fellowship at the University of Wuerzburg, she became Principal Investigator in the Department of Medicine at the University of Muenster, Germany. In 2006 Dr. Schaefer was recruited as a full professor of nephropharmacology at the Institute of Pharmacology and Toxicology, Goethe University. Her laboratory has investigated the role of the two small leucine-rich proteoglycans (SLRPs), decorin and biglycan, in acute inflammation, innate immunity and renal fibrosis. Dr. Schaefer has made significant contributions to the field of innate immunity by discovering that both SLRPs, when in soluble form in the blood and body fluids, can act as endogenous “danger” signals and thus directly involved in modulating the activity of Toll-like receptors
Charles Streuli MA, PhD
Charles Streuli's scientific achievements have been to discover mechanisms by which cell-matrix interactions control developmental morphogenesis, survival and proliferation, as well as tissue-specific gene expression, in epithelial tissues. By focusing on breast biology, he revealed the central role of integrin adhesion receptors in mammalian cell behaviour, providing a general framework for understanding epithelial tissue development and function.
He discovered that integrins control cellular differentiation, and identified a molecular pathway linking integrins with tissue-specific gene expression. His laboratory also revealed that cell-matrix interactions determine apoptosis by controlling Bax trafficking between cytosol and mitochondria. Charles’ group further discovered that integrins determine the orientation of cellular polarity in breast, and that this occurs via endocytosis of apical components away from cell-matrix adhesions.
Now Dr. Streuli is evolving completely novel areas of research on cell-matrix interactions. He is determining how the micro-mechanics of breast tissue has a central role in starting cancer in women, as well as the links between cell-matrix adhesion and circadian clocks in breast biology. He is also investigating how the small GTPase, Rac1, contributes to breast development and cancer.