Collectively, the data demonstrated that HA can serve as a signal integrator by facilitating TGF-beta11-mediated CD44-EGF-R-ERK interactions and ultimately regulate fibroblast phenotype. I propose a model to explain this novel mechanism and the functional consequence of age-dependent dysregulation. This mechanism may have direct implications for modifying the wound healing response, particularly for developing therapeutic strategies to improve healing in the elderly.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:585036 |
| Date | January 2010 |
| Creators | Simpson, Russell Michael Lloyd |
| Publisher | Cardiff University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://orca.cf.ac.uk/55467/ |
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