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Inflammation in wound repair and cancer

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Dates:29 September 2015
Times:13:00 - 14:00
What is it:Seminar
Organiser:Faculty of Life Sciences
Who is it for:University staff, Current University students
Speaker:Professor Paul Martin
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  • In category "Seminar"
  • In group "(FLS) Tissue Systems Seminar Series"
  • By Faculty of Life Sciences

We model wound healing in several genetically tractable model organism from the fruitfly, Drosophila, through to mice. We know that inflammation causes fibrosis and is aberrant in chronic wounds and so we use Drosophila and the translucent Zebrafish to make movies of leukocyte migration into the wound and to dissect the genetics of inflammatory cell recruitment towards tissue damage. In Drosophila and mice we have used array approaches to identify inflammation-dependent wound gene inductions. One such inflammation-dependent gene is osteopontin; we find that if osteopontin is “knocked-down” at the wound site, then repair is faster and scarring is significantly reduced. We have also identified a family of genes, the Ephs and ephrins that appear important for loosening up cell:cell adhesions to allow efficient wound re-epithelialisation. Each of these wound gene pathways have direct implications for development of therapeutics for improving wound repair in the clinic, either by reducing scarring at the wound site, or kick-starting of chronic wounds. Recently, we have also begun investigating parallels between wound healing and cancer. Just as for wounds, we find H2O2 to be a primary attractant enabling immune cells to sense early clones of transformed cells before they progress to cancers. We find that clones of transformed cells deprived of immune cells proliferate at a slower rate suggesting that growth signals, which include prostaglandins, are delivered to the transformed cells by immune cells. This observation may, in part, explain recent studies showing how low dose aspirin can stave off the onset of gut and other cancers. Since surgery is one of the most effective means of treating cancer we have begun to use zebrafish to model cancer surgery, in particular investigating how the wound inflammatory response impacts on immune cell recruitment to nearby transformed cells and what might be the downstream consequences of this.

Speaker

Professor Paul Martin

Organisation: University of Bristol

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Michael Smith Lecture Theatre
Michael Smith Building
Manchester

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Charlotte Houghton

0161 275 5360

charlotte.houghton@manchester.ac.uk

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