Ishibe S et al. - Epithelial de-differentiation after kidney injury or in epithelial culture systems is controlled by secreted factors such as transforming growth factor [beta] and hepatocyte growth factor as well as cell-cell and cell-matrix interactions. These surface signals stimulate intracellular signaling via the mitogen-activated protein kinase, phosphoinositide-3-kinase, and Wnt/[beta]-catenin pathways that in turn activate the morphologic and transcriptional events involved in cell spreading, migration, and proliferation. As cell confluency increases during the repair process, and the factors stimulating de-differentiation are suppressed, these morphogenic programs are downregulated and signals to promote re-differentiation are activated.
