Dr Ana Tiganescu
I obtained my BSc in Biological Sciences at the University of Warwick in 2005 and developed strong molecular biology laboratory skills through employment at the University of Oxford Weatherall Institute for Molecular Medicine and Wellcome Trust Centre for Human Genetics. After a year nanotechnology industry (Oxonica Ltd.) developing novel biodiagnostic assays and UV suncream enhancers, I joined the University of Birmingham and completed my PhD on Glucocorticoid Metabolism in Ageing Skin in 2011. I then undertook a 2-year Visiting Research Scholarship at the University of California San Francisco where I developed in vivo models of wound healing.
In 2014 I joined the University of Leeds where I continue my research as an Independent Academic Fellow.
At the interface between Endocrinology and Dermatology, my research applies knowledge of hormonal pathways to advance therapies for impaired skin function. Over the past 10 years, I have pioneered a novel regulatory pathway in skin: pre-receptor regulation of glucocorticoid (stress hormone) signalling through 11β-hydroxysteroid dehydrogenase enzyme action in skin ageing, wound healing, UVB exposure and glucocorticoid toxicity. My mission is to establish myself as an independent inter-disciplinary scientist, developing new therapies to improve skin function across a spectrum of research interests.
My research is focused on 11β-HSD isozymes which regulate local glucocorticoid availability. During my PhD at the University of Birmingham (2007-2011), I was the first to characterize the ability of 11β-HSD1 to generate cortisol from cortisone in the skin and found increased expression and activity during skin ageing. I demonstrated that mice with a global 11β-HSD1 deletion were protected from age-induced dermal atrophy and improved collagen processing. My post-doctoral studies at the University of California San Francisco (2012-2014) identified a role for 11β-HSD1 in wound healing and demonstrated that treatment with a topical 11β-HSD1 inhibitor prevented cutaneous effects of steroid toxicity including skin thinning and delayed wound healing. In 2014 I joined the In 2014 I joined the University of Leeds as an Independent Academic Research Fellow where I secured an MRC Confidence in Concept Award to investigate 11β-HSD1 inhibition as a novel therapy for wound healing in type 2 diabetes (https://doi.org/10.1186/ISRCTN74621291).
- PhD Medicine
- BSc Biological Sciences
- School of Medicine Research Ethics Committee
- STEM Ambassador
- Society for Investigative Dermatology
- Society for Endocrinology
- Endocrine Society
I am primary supervisor for a PhD student (Padiporn Limumpornpetch who is a visiting endocrinologist from Thailand. She recently completed her second year and is investigating the interplay between inflammation, hypoxia and cortisol metabolism in human skin.
My teaching commitments include several research and fundamental biology modules on the MBChB degree.
I am also a registered STEM Ambassador and enjoy inspiring the next generation of scientists.
Research groups and institutes
- Discovery and Translational Science
- Leeds Institute of Cardiovascular and Metabolic Medicine
- Musculoskeletal disease
- Translational and clinical research
- Dermato-Rheumatology Group
<li><a href="//phd.leeds.ac.uk/project/246-cellular-conversations:-stress-hormone-metabolism-as-a-novel-anti-fibrotic-target-in-giant-cell-arteritis">Cellular conversations: stress hormone metabolism as a novel anti-fibrotic target in Giant Cell Arteritis</a></li>
<li><a href="//phd.leeds.ac.uk/project/684-hypoxia,-inflammation-and-local-steroid-metabolism-during-wound-healing:-towards-a-new-therapy-for-diabetic-foot-ulcers">Hypoxia, inflammation and local steroid metabolism during wound healing: towards a new therapy for diabetic foot ulcers</a></li>
<li><a href="//phd.leeds.ac.uk/project/685-regulation-of-skin-function-and-wound-healing-by-pre-receptor-glucocorticoid-metabolism-in-diet-induced-animal-models-of-diabetes">Regulation of skin function and wound healing by pre-receptor glucocorticoid metabolism in diet-induced animal models of diabetes</a></li>