Ewch i’r prif gynnwys
Dr Robert Steadman

Dr Robert Steadman

Senior Lecturer

Yr Ysgol Meddygaeth

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

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                 

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.

Aelodaethau proffesiynol

  • 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.

Pwyllgorau ac adolygu

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          

2019

2017

2016

2015

2014

2013

2011

2010

2009

2008

2007

2006

2004

2003

2002

2001

1999

1998

1997

1996

1995

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.