Modelling the cell biology of wound healing in flies and in silico.
Lead Research Organisation:
University of Bristol
Department Name: Biochemistry
Abstract
Abstract
(no more than 4,000 characters inc spaces)
Effective wound re-epithelialisation and an accompanying robust inflammatory response are critical for the survival of most organisms. The two extreme pathologies of aberrant healing are chronic wound healing (e.g. diabetic foot ulcers) and fibrotic scarring. A better understanding of the molecular and cellular mechanisms driving normal healing will guide us how these processes can be modulated in the clinic to accelerate tissue repair.
Recently, our collaborations with mathematical modellers have enabled us to determine otherwise impossible-to-unravel characteristics of the wound attractants that draw in the inflammatory response and these have indicated potential new prognostic markers for stratifying chronic wounds into healers versus "stubborn" healers. Here, we are using a similar approach, integrating experimental in vivo biology and mathematical modelling to uncover more details about the mechanisms driving wound repair. By integrating live in vivo confocal imaging in translucent Drosophila pupae with cutting-edge biophysical mathematical modelling, we are gaining novel insight into how epithelial tissues repair wounds. For example, we are interested in how global mechanical signals within the epithelium, as well as more local cytoskeletal drivers in the front row cells and cell:cell interactions (both at the leading edge and many rows further back) will together influence the repair process. Crucially, the mathematical modelling will simulate real in vivo data gathered from Drosophila wound studies and provide "predictive" feedback insights that will guide further biology experiments.
For translational relevance, our studies will be integrated with clinical studies using patient wound samples (biopsy material from wounds that do and don't subsequently heal) provided by our clinical collaborators (Cardiff).
(no more than 4,000 characters inc spaces)
Effective wound re-epithelialisation and an accompanying robust inflammatory response are critical for the survival of most organisms. The two extreme pathologies of aberrant healing are chronic wound healing (e.g. diabetic foot ulcers) and fibrotic scarring. A better understanding of the molecular and cellular mechanisms driving normal healing will guide us how these processes can be modulated in the clinic to accelerate tissue repair.
Recently, our collaborations with mathematical modellers have enabled us to determine otherwise impossible-to-unravel characteristics of the wound attractants that draw in the inflammatory response and these have indicated potential new prognostic markers for stratifying chronic wounds into healers versus "stubborn" healers. Here, we are using a similar approach, integrating experimental in vivo biology and mathematical modelling to uncover more details about the mechanisms driving wound repair. By integrating live in vivo confocal imaging in translucent Drosophila pupae with cutting-edge biophysical mathematical modelling, we are gaining novel insight into how epithelial tissues repair wounds. For example, we are interested in how global mechanical signals within the epithelium, as well as more local cytoskeletal drivers in the front row cells and cell:cell interactions (both at the leading edge and many rows further back) will together influence the repair process. Crucially, the mathematical modelling will simulate real in vivo data gathered from Drosophila wound studies and provide "predictive" feedback insights that will guide further biology experiments.
For translational relevance, our studies will be integrated with clinical studies using patient wound samples (biopsy material from wounds that do and don't subsequently heal) provided by our clinical collaborators (Cardiff).
Organisations
People |
ORCID iD |
| Paul Martin (Primary Supervisor) | |
| Jake Turley (Student) |