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Dr Robert Steadman

Dr Robert Steadman

Senior Lecturer, School of Medicine

Email
steadmanr@cardiff.ac.uk
Telephone
+44 (0)29 2074 8390
Campuses
UHW Main Building

Overview

Between 10-15% of the world population has Chronic Kidney Disease, characterized by progressive scarring of the kidney. My research addresses the mechanisms underlying the injury and progression of this scarring. Our focus is on understanding the cell- cell and cell-extracellular matrix interactions that control scarring and fibrosis. These interactions are similar to those involved in normal wound healing and by contrasting wound healing and fibrotic responses we have identified several novel potential therapeutic targets.

I am Outreach and Dissemination Lead of Wales Kidney Research Unit, a Biomedical Research Unit funded by Health and Care Research Wales to deliver an All-Wales strategy for the study, diagnosis, prevention, treatment and social context of kidney disease. See: http://kidneyresearchunit.wales/en/

Grant review

I peer-review grant applications for:

MRC

Kidney Research UK

The Wellcome Trust

University committees

2005-present.  Cardiff Institute of tissue Engineering and Repair (CITER) Learning and Teaching Committee   Member

2005-present.  CITER MSc in Tissue Engineering Programme Committee. Vice-Chair

2007 - 2016.  School of Medicine Research Degrees Committee. Member

2007 - 2016.  School of Medicine, Postgraduate Course in Biomedical Research Techniques Advisory Group. Chair

Biography

Education/Qualifications

1989, PhD; University of Wales, Cardiff.

1986, MSc; University of Birmingham, Birmingham

1978, BSc; University of Wales, Aberystwyth

Career overview

1993-1997    Lecturer in Cell Biology, Institute of Nephrology, University of Wales College of Medicine, Royal Infirmary, Cardiff, UK

1992-1993    Postdoctoral Research Fellow, Institute of Nephrology, University of Wales College of Medicine, Royal Infirmary, Cardiff, UK

1990-1992    Visiting Senior Fullbright Scholar, Department of Cell Biology and Anatomy, University of Alabama at Birmingham, Alabama, USA.

Professional memberships

  • Biochemical Society

    The Renal Association

    British Society for Matrix Biology

    Tissue and Cell Engineering Society

    Society for Endocrinology

Member of the Cardiff Institute of Tissue Engineering and Repair.

Committees and reviewing

2005-present. Cardiff Institute of tissue Engineering and Repair (CITER) Learning and Teaching Committee   Member

2005-present.  CITER MSc in Tissue Engineering Programme Committee. Vice-Chair

2007-2016.  School of Medicine Research Degrees Committee. Member

2004-2016.  School of Medicine, Postgraduate Course in Biomedical Research Techniques. Director

2009-2016.  School of Medicine, Master of Research in Biomedical Research. Director

2014-2016.  School of Medicine, MSc in Medical Research and Innovation. Director

Publications

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1988

The research of my group focuses on understanding the common mechanisms controlling the processes of wound healing, scarring and fibrosis. These all centre on the induction and function of the myofibroblast. This cell is not present in normal tissue but differentiates either from endogenous cells, such as fibroblasts or epithelial cells or from circulating fibrocytes that are targeted to sites of tissue remodelling. This differentiation is under the influence of growth factors such as transforming growth factor (TGF)b1 and this is central to the pathological process.

Fibroblasts are cells that populate the connective tissue of most organs of the body. When they take up a myofibroblast phenotype they lose their spindle-shaped morphology and become large contractile cells. They develop intracellular actin stress fibres that incorporate a-smooth muscle actin (a-sma) and allow the cell to contract, closing the wound or pulling scar-tissue together. This process is essential to healing skin wounds but pathological when it happens in a solid organ such as the kidney, lungs or liver.

Our current focus on the glycosaminoglycan hyaluronan began with the observation that hyaluronan was incorporated into large pericellular matrices when a fibroblast differentiated into a myofibroblast (Jenkins et al JBC, 2004). Delineating the mechanisms regulating this and assigning a role to this matrix has revealed that there is a causal relationship between hyaluronan assembly and cell phenotype . We are now at the point where we’re beginning to understand some of the factors that are involved in controlling the hyaluronan-dependent regulation of cell phenotype and have begun to fill the mechanistic gaps in our understanding.

Supervision

Past projects