Fibrosis is a disease which is characterised by scarring of tissues due to excessive production of extracellular matrix molecules. It has been described as unresolved wound healing. Previous studies have implicated IGFBP-5 and TGF-β1 as pivotal players in fibrosis. This study was undertaken to compare the effects of IGFBP-5 and TGF-β1 , with respect to one particular aspect of the response injury, epithelial mesenchymal transition (EMT). 1 developed Epithelial and Mesenchymal clones from NMuMg (epithelial) cells which were characterised by morphology and by expession of cell-surface markers. The ability of the Epithelial clone to undergo EMT with TGF-β1 and its increased sensitivity to TGF-β1 treatment compared with their mesenchymal counterparts made it an effective model to examine the effects of IGFBP-5. lGFBP-5 was not able to drive an EMT process since it failed to decrease E-cadherin expression (a marker of epithelial cells) and downregulated fibronectin expression (a mesenchymal marker) in mesenchymal clones.EThOS - Electronic Theses Online ServiceGBUnited Kingdo