Dr Maryse Bailly
Institute of Ophthalmology
Faculty of Brain Sciences
- Joined UCL
- 1st Dec 2000
My group uses a range of cellular models to study physiological and pathological cell behaviour regulated by actin dynamics in the context of tissue contraction and scarring. The common long-term goal of these studies is to identify basic molecular mechanisms to uncover new specific targets to modulate scarring and fibrosis in a range of diseases as well as within cell repair and regeneration processes. The lab most recent interests broadly fall under two areas:
1) Mechanisms of fibroblast-mediated contraction in wound healing and fibrosis:
Tissue contraction and scarring processes play a part in the pathogenesis or failure of treatment of virtually every major blinding disease, and are also a major cause of morbidity in the whole human body. Yet, very little is known about the molecular mechanisms involved and there are no treatment available for ocular scarring besides toxic anti-cancer drugs with limited use. My group has developed over the last 10 years in vitro and ex vivo models that allow the study tissue contraction mechanisms within pseudo-physiological 3D “tissue-like” environments. Focusing on ocular diseases, the group has used these models to characterise the biology of the contraction process and the molecular pathways underlying conjunctiva contraction, identifying novel targets such as the Rac1 small GTPase to develop promising anti-scarring agents. More recently we have extended this work to specific eye diseases with a major fibrotic component such as Floppy Eye Lid Syndrome (FES), Thyroid Eye Disease (TED) and recurrent trachomatous trichiasis (TT), where the disease mechanisms are unknown and no good treatment is available. These studies have identified a specific molecular signature underlying the fibrotic disease phenotype, and demonstrated that the diseased cells display specific alterations in their mechanical properties that underlie they ability to contract tissues and promote scarring.
2) Tensional homeostasis, mechanical stress and modulation of the SRF/MRTF-A pathway in fibrosis:
Mechanical sensing is a fundamental process that regulates essential cellular features such as shape, motility, proliferation or differentiation. Deregulation of the tissue tensional homeostasis in stromal cells is at the basis of most stress-induced pathological remodelling, such as cardiac hypertrophy, fibrosis and scarring. We have recently identified Myocardin-Related Transcription Factor-A (MRTF-A), the major co-activator for the Serum Response Factor (SRF) transcription factor, as a biosensor for tensional homeostasis in cells. Our goal is now to identify the mechanisms by which cells measure their internal tension and what actually determines the intrinsic tensional homeostasis level in individual cells, and the role of the MRTF-A/SRF pathway in the process.
I teach a number of lectures at UCL, broadly around cytoskeleton, models and imaging.
CELL0016- Actin cytoskeleton and Intermediate Filaments
CELL0017 Fibrosis and mechanotransduction
CELL0009- CELL0010: Models organisms and techniques
MSc Biomaterials & Tissue Engineering
- Universite Claude Bernard (Lyon 1)
- Doctorate, Doctor of Philosophy | 1992
- Universite Claude Bernard (Lyon 1)
- Other Postgraduate qualification (including professional), Diplome Universitaire de Technologie | 1983
1992 - 1993 Postdoctoral Fellow, Laboratoire d'Immunologie et de Cancérologie Expérimentale, Centre Léon Bérard, Lyon, France
1993 - 1995 Postdoctoral Fellow, Laboratoire d'Oncologie Moléculaire, Centre Léon Bérard, Lyon, France
1995 – 2000 Research Associate, Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, New York
2000 –2006 Lecturer in Cell Biology and Wound Healing, Institute of Ophthalmology, University College London and Honorary Lecturer of The Moorfields Eye Hospital