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Transdifferentiation


Transdifferentiation, also known as lineage reprogramming, is a process in which one mature somatic cell transforms into another mature somatic cell without undergoing an intermediate pluripotent state or progenitor cell type. It is a type of metaplasia, which includes all cell fate switches, including the interconversion of stem cells. Current uses of transdifferentiation include disease modeling and drug discovery and in the future may include gene therapy and regenerative medicine. The term 'transdifferentiation' was originally coined by Selman and Kafatos in 1974 to describe a change in cell properties as cuticle producing cells became salt-secreting cells in silk moths undergoing metamorphosis.

Davis et al. 1987 reported the first instance of transdifferentiation where a cell changed from one adult cell type to another. Forcing mouse embryonic fibroblasts to express MyoD was found to be sufficient to turn those cells into myoblasts.

There are no known instances where adult cells change directly from one lineage to another except Turritopsis dohrnii. Rather, cells dedifferentiate and then redifferentiate into the cell type of interest. In newts when the eye lens is removed, pigmented epithelial cells de-differentiate and then redifferentiate into the lens cells.

While it was previously believed that oesophageal cells were developed from the transdifferentiation of smooth muscle cells, that has been shown to be false.

The first example of functional transdifferentiation has been provided by Ferber et al. by induce a shift in the developmental fate of cells in liver and convert them into 'pancreatic beta-cell-like' cells. The cells induced a wide, functional and long-lasting transdifferentiation process that reduced the effects of hyperglycemia in diabetic mice. Moreover, the trans-differentiated beta-like cells were found to be resistant to the autoimmune attack that characterizes type 1 diabetes.


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