Dr Sarah Herrick

Faculty of Life Sciences
3.239 Stopford Building
The University of Manchester
Oxford Road
Manchester
M13 9PT

Tel:     +44 (0) 161 275 6765

email:  sarah.herrick@manchester.ac.uk

http://www.ls.manchester.ac.uk/people/profile/index.asp?id=1512

Research Profile

Tissue repair
The overall goal of our studies is to understand the fundamental cellular and molecular mechanisms involved in normal turnover of extracellular matrix molecules during tissue repair, the way these processes are altered leading to excessive healing (scarring/fibrosis) or delayed healing (chronic wounds) and to identify ways of regulating these processes therapeutically. We are using a number of experimental systems including cell culture assays, in vivo animal models and human biopsy tissue analysis, as well as a range of cellular, histological, molecular and biochemical techniques to elucidate mechanisms regulating these tissue repair disorders.

Peritoneal repair and adhesion formation
An extremely common problem of surgery in the abdomen is peritoneal adhesion formation where organs, which should normally be separate, become joined by fibrous bands of tissue. Peritoneal adhesions can cause major complications such as intestinal obstruction, chronic pelvic pain and infertility in women. However, little is known about how adhesions form, how they mature and how they are broken down naturally in the body. Our previous histological and ultrastructural studies have shown that adhesions were well vascularised and surprisingly well innervated. We also found that the omentum or ‘policeman of the abdomen’ was more often that not involved in adhesion development. Our current studies are aimed at understanding the role of the initial wound matrix, deposited as a fibrin-rich clot between injured surfaces, and the fibrinolytic proteases involved in its breakdown. We have shown that this provisional fibrin matrix plays a major role in regulating collagen production both in tissue culture assay systems and in vivo models. Furthermore, our recent studies suggest that a defect in fibrin removal results in an even greater accumulation of collagen which we think leads to subsequent fibrosis and adhesion formation.

Improved tissue-engineered skin replacements
One way of treating chronic non-healing wounds as well as other wound healing defects such as burns is by covering them with a skin graft. These grafts may be from the patient’s own skin or engineered artificially. Most tissue-engineered skin replacements consist of a dermal and a surface epidermal layer but lack a lower subcutaneous fat component. Problems can occur if the graft is rejected due to poor vascularisation or if over time, scarring develops leading to loss of tissue function. Little work has been done to study the interaction of cells in the different skin layers, in particular, the role of the subcutaneous cells in directing the growth of vascular and neural networks and preventing excess scarring. Our overall aim is to generate the next generation of skin replacements that have improved graft take and better integration with host tissue. This work is being carried out in collaboration with the UK Centre for Tissue Engineering, directed by Professor Tim Hardingham.