Dr Jenna Cash

Jenna Cash's research focuses on understanding the events that determine whether a skin wound will heal acutely or develop into a chronic non-healing wound.

Dr Jenna Cash

Chancellor's Fellow and Sir Henry Dale Fellow

  • Centre for Inflammation Research

Contact details

Group Members

Yonlada Nawilaijaroen, Research Assistant

Ishita Dasgupta, BSF PhD student

Pruistinne Harijanto, Research Assistant

Charlotte Dawson, Visiting Postdoctoral Research Assistant

Oliver Davis, MScR student

Roseanne Khawaja, MScR student

Vignesh Jayaraman, PhD student (2nd supervisor with Dr Tovah Shaw)

Erqing Gao, PhD student (2nd supervisor with Prof Suhong Xu)

Background

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​Multiphoton image of mouse skin with CD68+ macrophages (green), CD31+ blood vessels (red) and collagen (second harmonics; grey)
Multiphoton image of mouse skin with CD68+ macrophages (green), CD31+ blood vessels (red) and collagen (second harmonics; grey).

The majority of skin wounds progress uneventfully through the sequential phases of healing, with the magnitude of the inflammatory response linked to the extent of the resultant scar. However, chronic wounds, including venous leg ulcers, diabetic foot ulcers and pressure ulcers, are thought to become 'stuck' in a chronically inflamed state, unable to heal effectively. Multiple immune and stromal cells, including macrophages, neutrophils, lymphocytes and keratinocytes play important roles in physiological and, most likely, pathophysiological healing. Macrophages are phenotypically plastic cells implicated both in supporting the 'normal' repair process, assisting angiogenesis, lymphangiogenesis and collagen deposition, and in playing detrimental roles in aberrant healing scenarios, with studies indicating that macrophages are dysfunctional, exhibiting unrestrained activation in the context of impaired healing in mouse and human. However, we lack a full appreciation of the dynamics of monocyte-macrophage recruitment and phenotype in acute skin wounds and macrophage biology has never been studied in a genetically tractable mammalian model of chronic wounds. An improved understanding of the acute repair program and how it becomes deranged to generate chronic wounds is urgently needed to inform new wound therapeutics. Exploiting resolution pathways may provide novel therapeutic strategies to stem the growing patient and healthcare burden that healing disorders inflict, perhaps by triggering resolution of chronic inflammation in non-healing wounds or reducing fibrosis.

Research Overview

The Cash lab has three linked programs of research that revolve around understanding the mechanisms that govern skin repair versus repair failure:

  1. Defining macrophage heterogeneity and function in acute and chronic skin wounds. Skin wounds typically heal uneventfully with scar formation, however, a growing number develop into non-healing wounds which become stuck in a chronically inflamed state, unable to heal effectively. Macrophages aid repair and resolution of tissue damage but are thought to become dysfunctional in chronic wounds. In order to define the role of macrophage subsets in repair outcome, we are identifying and characterising macrophage populations, including the dynamics of their recruitment, phenotype and emigration signatures in acute and chronic wounds.
  2. Harnessing pro-resolving pathways to drive skin repair Pro-resolving pathways direct the termination of the inflammatory response. We are exploring whether specific resolution pathways can be targeted to therapeutically accelerate acute wound repair with reduced scarring and/or rescue derailed repair responses.
  3. Skin vascular niche Restoration of blood flow to damaged tissues provides the oxygen and nutrients required to facilitate wound healing. Dysregulated angiogenesis plays a prominent role in the non-healing nature of chronic wounds. We are investigating the impact of wound microenvironment on the skin vascular niche in order to develop therapeutic strategies to promote optimal neovascularisation.

We use a variety of complementary approaches, including single-cell spatial multiomic profiling, scRNAseq, immunohistochemistry, multiphoton imaging and precision cut skin slice culture. We also take advantage of in vitro assays and human wound biopsies to help dissect mechanism and provide translational relevance.

The lab is supported by multiple grants including funding from industry collaborators, Wellcome Trust, Royal Society, UKRI and the British Skin Foundation. Dr. Cash also founded and chairs Ed-SKIN, an inter-disciplinary group with over 80 members and an annual symposium. In 2025, Ed-SKIN is twinning with SKINTEGRITY.CH, with joint meetings scheduled to start in Autumn 2025.

Skin Repair Lab website

Edinburgh Skin Network website

Document
Cash Group graphic summary (510.19 KB / PDF)

Biographical Profile

Dr Jenna Cash graduated from the University of Edinburgh with a 1st class degree in Pharmacology (with Industrial Experience) in 2005. She was then awarded a 4-year British Heart Foundation DPhil studentship at the Sir William Dunn School of Pathology, Oxford University, with Professor David Greaves. Her DPhil research resulted in the discovery that a protein, chemerin, undergoes proteolytic processing by activated macrophages to generate peptides with dual anti-inflammatory and pro-resolving properties. Chemerin-derived peptides are under international patent and underwent clinical trials to treat skin inflammation.

On completion of her DPhil, Dr. Cash was awarded a Sir Henry Wellcome Postdoctoral Fellowship for 4 years, which she divided between Professor Mauro Perretti's lab (William Harvey Research Institute, London), Professor Paul Kubes lab (Calgary University, Canada) and Professor Paul Martin's lab (Bristol University). During this period she learnt specialised intravital microscopy techniques and developed a keen interest in wound healing, finding that chemerin peptide C15 can accelerate skin repair with reduced scarring and inhibit neutrophil integrin activation to reduce their recruitment to a site of inflammation.

Dr. Cash was subsequently awarded an Elizabeth Blackwell Early Career Research Fellowship by Bristol University/Wellcome ISSF before moving to the University of Edinburgh where she is now a Chancellor's Fellow at the Centre for Inflammation Research, Institute for Regeneration and Repair. She held a Sir Henry Dale Fellowship from the Wellcome Trust/Royal Society from 2016 to 2023, which established her lab within the Centre for Inflammation Research. Her research continues to focus on understanding wound healing mechanisms and developing novel therapeutic approaches for chronic wounds.

Honours and Awards

  • Physiological Society Travel Award, 2015
  • Emerging Investigator Prize, London Matrix Symposium, 2013
  • Outstanding Young Investigator Award, William Harvey Research Institute Symposium, 2011
  • Poster Prize at the World Congress on Inflammation, Tokyo, 2009
  • BHF Centre of Research Excellence Travel Award, 2009
  • Young Immunologist of the Year Award, British Society for Immunology Congress, Glasgow, 2008

Alumni

  • Vel Shinkov
  • Christos Mavrommatis
  • Valentina Moreno Mitchell
  • Yashna Rambeerich
  • Katie Tse
  • Dr Holly Rocliffe
  • Dr Antonella Pellicoro
  • Swati Shaji
  • Emma Guy
  • Giulia Bartolomucci
  • Dr Shani Austin-Williams 
  • Dr Georgios Krilis
  • Ms Danielle Shields
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Image of a petri dish covered in microbial growth
Microbial handprint

Public Engagement

As a Science, Technology, Engineering and Mathematics (STEM) Ambassador since 2010 I previously volunteered at public engagement events such as Centre of the Cell (London). On moving to the CIR, I have become involved in the Science Festivals subcommittee of our Public Engagement team as co-lead.  I am particularly interested in discussing wound repair, including raising awareness of chronic wounds and visit primary schools in East Lothian to run ‘Meet the Microbes’ sessions, whereby the children grow their own microbial handprints on agar plates whilst learning of the importance of effective handwashing in relation to the role of microbes in disease.

Collaborators