Flightless I deficiency enhances wound repair by increasing cell migration and proliferation

Simple item page
dc.contributor.authorCowin, A.
dc.contributor.authorAdams, D.
dc.contributor.authorStrudwick, X.
dc.contributor.authorChan, H.
dc.contributor.authorHooper, J.
dc.contributor.authorSander, G.
dc.contributor.authorRayner, T.
dc.contributor.authorMatthaei, K.
dc.contributor.authorPowell, B.
dc.contributor.authorCampbell, H.
dc.contributor.organisationCentre for the Molecular Genetics of Development
dc.date.issued2007
dc.descriptionCopyright © 2007 Pathological Society of Great Britain and Ireland The definitive version may be found at www.wiley.com
dc.description.abstractWound healing disorders are a therapeutic problem of increasing clinical importance involving substantial morbidity, mortality, and rising health costs. Our studies investigating flightless I (FliI), a highly conserved actin-remodelling protein, now reveal that FliI is an important regulator of wound repair whose manipulation may lead to enhanced wound outcomes. We demonstrate that FliI-deficient + /- mice are characterized by improved wound healing with increased epithelial migration and enhanced wound contraction. In contrast, FliI-overexpressing mice have significantly impaired wound healing with larger less contracted wounds and reduced cellular proliferation. We show that FliI is secreted in response to wounding and that topical application of antibodies raised against the leucine-rich repeat domain of the FliI protein (FliL) significantly improves wound repair. These studies reveal that FliI affects wound repair via mechanisms involving cell migration and proliferation and that FliI might represent an effective novel therapeutic factor to improve conditions in which wound healing is impaired.
dc.description.statementofresponsibilityAJ Cowin, DH Adams, XL Strudwick, H Chan, JA Hooper, GR Sander, TE Rayner, KI Matthaei, BC Powell, HD Campbell
dc.identifier.citationJournal of Pathology, 2007; 211(5):572-581
dc.identifier.doi10.1002/path.2143
dc.identifier.issn0022-3417
dc.identifier.issn1096-9896
dc.identifier.orcidCowin, A. [0000-0003-2885-2080]
dc.identifier.urihttp://hdl.handle.net/2440/41536
dc.language.isoen
dc.publisherJohn Wiley & Sons Ltd
dc.source.urihttps://doi.org/10.1002/path.2143
dc.subjectflightless I
dc.subjectactin
dc.subjectcytoskeleton
dc.subjectwound
dc.subjectskin
dc.subjectfibrosis
dc.subjectscar
dc.titleFlightless I deficiency enhances wound repair by increasing cell migration and proliferation
dc.typeJournal article
pubs.publication-statusPublished

Files

Collections

Surgery publications
Centre for the Molecular Genetics of Development publications