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Role of transglutaminases in signalling that regulates epithelial responses in wound healing

This thesis has investigated the mechanisms by which re-epithelialisation occurs with regard to TG2. In the first stage of wound healing, an influx of growth factors and metalloproteinases occurs, that through the initial interaction of TG2 are able to stabilise the matrix and stimulate keratinocyte cells to migrate and proliferate to close the wound. Experiments have indicated that TG2 is able to stimulate proliferation and migration of keratinocyte cells both directly and indirectly by modulating metalloproteinase signalling, leading to the activation of the EGFR by EGF ligands liberated from the ECM. Furthermore, through the course of altering TG2's conformation and activity experiments have determined that TG2 must be in an open and active conformation in order for it to affect keratinocyte signalling leading to proliferation and migration. Finally, a G protein coupled receptor has been investigated as to whether it may be involved in TG2 driven proliferation and migration in keratinocytes. Previous work by Xu et al., 2006 had shown TG2 binds to GPR56 and this GPCR has been shown to be involved in proliferation and migration of cells located in the brain and heart. Although investigations of GPR56 are at this time inconclusive regarding keratinocytes proliferation and migration this thesis confirms the presence of GPR56 in keratinocytes. Therefore GPR56 may be involved in keratinocyte migration and proliferation