This item is available under a Creative Commons License for non-commercial use only
Through the use of developmental and knock out studies Mig-6 has been shown to have a role in development. It has also been shown to be a tumour suppressor gene. Little work has been done as yet looking at its role in the adult. This study examined the role of Mig-6 in the lung with the ultimate goal being to determine if the pulmonary phenotype due to Mig-6 ablation is due to a developmental programming or loss of function in the adult. This was investigated in two ways. 1. To investigate if knocking out Mig-6 in adult lung has an effect on lung function
2. Investigate the role of Mig-6 in lung epithelial cells by RNAi (Investigation of the Role of Mig-6 in Pulmonary Epithelial Cells and Vascular Cells In Vitro).
Knocking out Mig-6 in the adult mice showed no difference in epithelial markers and after staining morphology and airway size were found to be normal. This would seem to indicate that the Mig-6 phenotype is due to altered development of the lungs during the neonatal period and not due to a loss of function in the adult. From the cell work we observed differences in the effect on epithelial cells vs. endothelial
cells when Mig-6 was knocked out. The epithelial cells showed an increased number of viable cells present after knocking out Mig-6 while the number of viable cells was decreased in the endothelial cells. This would indicate that knocking out Mig-6 in epithelial cells causes increased proliferation but in endothelial cells causes apoptosis. Conclusions: Ablation of Mig-6 leads to increased proliferation in epithelial cells (and
apoptosis in endothelial cells) but knocking it out in the adult stage has a mild effect on lung
Bennett, S.:Mig-6 and Its Role in Regulating Adult Lung Epithelium. M. Phil. thesis. Dublin Institute of Technology, 2010.