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* Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, Bethesda, Maryland
20892-5431; and Thyroid hormone (T3 or 3,5,3 Department of Immunology, Holland Laboratory, American Red Cross, Rockville, Maryland 20855
-triiodothyronine) plays a causative role during amphibian metamorphosis. To investigate how T3 induces some cells to
die and others to proliferate and differentiate during
this process, we have chosen the model system of intestinal remodeling, which involves apoptotic degeneration of larval epithelial cells and proliferation and differentiation of other cells, such as the fibroblasts and
adult epithelial cells, to form the adult intestine. We
have established in vitro culture conditions for intestinal epithelial cells and fibroblasts. With this system, we
show that T3 can enhance the proliferation of both cell
types. However, T3 also concurrently induces larval epithelial apoptosis, which can be inhibited by the extracellular matrix (ECM). Our studies with known inhibitors of mammalian cell death reveal both similarities
and differences between amphibian and mammalian
cell death. These, together with gene expression analysis, reveal that T3 appears to simultaneously induce different pathways that lead to specific gene regulation,
proliferation, and apoptotic degeneration of the epithelial cells. Thus, our data provide an important molecular and cellular basis for the differential responses of
different cell types to the endogenous T3 during metamorphosis and support a role of ECM during frog
metamorphosis.
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