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Blizard Institute - Faculty of Medicine and Dentistry

Dr Emanuel Rognoni, BSc, MSc, PhD





I am a Biochemist by training and obtained my degree at the Technical University of Munich, Germany, in 2007 (BSc and MSc in Biochemistry). I then undertook a PhD (with summa cum laude) in Pharmacology at the Department for Molecular Medicine, Max Planck Institute of Biochemistry in Munich. My project focused on the Epidermal bullosa subtype Kindler Syndrome, exploring the role of the focal adhesion protein Kindlin-1 in skin development, homeostasis and skin cancer. For the research achievements of my PhD I was awarded the Junior Research Award of the Max Planck Institute and Young Investigator Award of the German Matrix Biology Society.

To extend my research track record in skin cell biology, I joined the lab of Prof Fiona Watt (Centre for Stem Cell and Regenerative Medicine, KCL) for my Postdoc in 2014 on an EMBO-long-term fellowship. My postdoctoral research focused on dissecting the plasticity and tissue scale behaviour of skin dermal fibroblast lineages during development, homoeostasis and wound healing. In 2018 I was awarded an EMBO advanced fellowship enabling me to expand my current research and transition to an independent position. At QMUL I first joined the Centre of Endocrinology as a lecturer in 2019 and then moved to the Centre for Cell Biology and Cutaneous Research at the Blizard Institute in 2022.

Undergraduate Teaching

Course Lecturer:  BMD311 - BSc Biomedical Science - Endocrine Physiology & Biochemistry 

Dissertation Supervisor: BIO603 - BSc Pharmacology - Project Skills in the Life Sciences

Project Supervisor: WHR6028 - iBSc Pharmacology & Innovative Therapeutics

Postgraduate Teaching

Course Lecturer: WHRM923- MRes Cardiac and Vascular Medicine 

Journal Clubs:  WHRM923- MRes Cardiac and Vascular Medicine 

Project Supervisor: MSc Regenerative Medicine

Project Supervisor: MSc Clinical Endocrinology


Research Interests:

The skin is our largest organ and most important protective barrier. It is constantly exposed to damage caused by injuries or environmental stress such as UV light induced sunburns. Skin repair requires coordinated function of two layers, the epidermis and dermis and perturbation of this process is associated with multiple skin diseases, ranging from fibrosis to cancer. The epidermis is a multi-layered (stratified) epithelium that is separated by a basement membrane from the underlying dermis. The dermis forms the skin scaffold consisting of a dense extracellular matrix (ECM) meshwork and different cell populations, including fibroblasts, sensory neurons, and endothelial and immune cells. During dermal development multipotent fibroblasts differentiate into distinct subpopulations that create the dermal sublayers, papillary, reticular and dermal white adipose tissue (DWAT). These fibroblast subpopulations differ in location and function and their cell identity and composition changes with age. This dermal maturation is governed by a tight balance of fibroblast proliferation, quiescence and ECM deposition. Our recent findings revealed that there is a coordinated switch in fibroblast behaviour of highly proliferative in embryonic development to quiescence postnatally allowing efficient ECM deposition/remodelling, which is necessary and sufficient to define dermal architecture.
While this postnatal quiescent state can be maintained long-term in postnatal skin, upon wounding different fibroblast lineages become activated at the wound site. These α-smooth-muscle-actin-(aSMA)-positive myofibroblasts quickly resume proliferation and migrate into the wound bed. Besides depositing/remodelling ECM in the wound bed, fibroblasts show astonishing plasticity and can acquire a dermal papilla or adipocyte fate in response to distinct signals promoting hair follicle and DWAT regeneration. After tissue repair, wound bed fibroblasts re-establish a quiescent state to maintain skin homeostasis. Deregulation of these complex developmental processes in the dermis is associated with several skin pathologies, including fibrosis, chronic wounds and cancer. 
Thus despite the fundamental role of fibroblasts in tissue maintenance and diseases, the extrinsic and intrinsic regulatory mechanisms controlling dermal fibroblast lineages behaviour and fate are largely unknown. In the lab we are pursuing a multidisciplinary approach to address the following key research questions: 

1.    How are fibroblast lineages specified and maintained throughout life?
2.    Which immune cell subtypes regulate fibroblast lineage behaviour and how are they influencing each other during skin development, regeneration and ageing? 
3.    What are the pathogenic processes promoting and maintaining aberrant fibroblast function in disease conditions? 

To answer these questions our lab is combining genome-wide screening, proteomics, in silico analysis, in vivo imaging, lineage tracing of dermal cells with multiple cell biology techniques. Our goal is to elucidate the fundamental biology defining fibroblast identity and plasticity during development, regeneration and disease paving the way for new treatment strategies targeting pathological fibroblast behaviour in skin diseases and potentially other organs. 



Key Publications

Rognoni E*, Goss G, Hiratsuka T, Sipilä KH, Kirk T, Kober KI, Lui PP, Tsang VS, Hawkshaw NJ, Pilkington SM, Cho I, Ali N, Rhodes LE, Watt FM*. Role of distinct fibroblast lineages and immune cells in dermal repair following UV radiation-induced tissue damage. Elife. 2021;10:e71052. (*corresponding author).

Rognoni E*, Pisco AO*, Hiratsuka T, Sipilä KH, Belmonte JM, Mobasseri SA, Philippeos C, Dilão R, Watt FM. Fibroblast state switching orchestrates dermal maturation and wound healing. Mol Syst Biol. 2018, 14(8), e8174. (*equal contribution).

Telerman SB*, Rognoni E*, Sequeira I, Pisco AO, Lichtenberger BM, Culley O, Viswanathan P, Driskell RR, Watt FM. Dermal Blimp1 acts downstream of epidermal TGFβ and Wnt/β-catenin to regulate hair follicle formation and growth.  J Invest Dermatol. 2017, 137(11), 2270-2281 (*equal contribution).

Rognoni E, Gomez C, Pisco AO, Rawlins EL, Simons BD, Watt FM, Driskell RR. Inhibition of β-catenin signalling in dermal fibroblasts enhances hair follicle regeneration during wound healing. Development. 2016, 143(14), 2522-35.

Rognoni E, Widmaier M, Jakobson M, Ruppert R, Ussar S, Katsougkri D, Böttcher RT, Lai-Cheong JE, Rifkin DB, McGrath JA, Fässler R. Kindlin-1 controls Wnt and TGF-β availability to regulate cutaneous stem cell proliferation. Nat Med. 2014, 20(4), 350-9.

All Publications


PhDs Primary Supervisor at Queen Mary

  • Mr Tom Kirk, PhD (2020 - present)
  • Mr Abubkr Abdelaal Ahmed, Barts PhD studentship (2021-present)
  • Ms Tjasa Bensa, BCSC Alexandra Carrell PhD studentship (start in April 2022)
  • Ms Stavroula Tekkela, BSF PhD studentship (start in September 2022)

PhDs secondary Supervisor at Queen Mary

  • Ms Anisha Rekha Mistry, PhD in Prof Márta Korbonits’ group (2019-present)
  • Ms Laura Gomez-Corral, PhD in Dr Carles Gaston-Massuet’s group (2020-present)
  • Ms Laura Forster, PhD in Dr Himardi Gupta’s group (start in September 2022)
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