Control of Müller glial cell proliferation and activation following retinal injury

MA Dyer, CL Cepko - Nature neuroscience, 2000 - nature.com
MA Dyer, CL Cepko
Nature neuroscience, 2000nature.com
Müller glial cells are the major support cell for neurons in the vertebrate retina. Following
neuronal damage, Müller cells undergo reactive gliosis, which is characterized by
proliferation and changes in gene expression. We have found that downregulation of the
tumor supressor protein p27 Kip1 and re-entry into the cell cycle occurs within the first 24
hours after retinal injury. Shortly thereafter, Müller glial cells upregulate genes typical of
gliosis and then downregulate cyclin D3, in concert with an exit from mitosis. Mice lacking …
Abstract
Müller glial cells are the major support cell for neurons in the vertebrate retina. Following neuronal damage, Müller cells undergo reactive gliosis, which is characterized by proliferation and changes in gene expression. We have found that downregulation of the tumor supressor protein p27 Kip1 and re-entry into the cell cycle occurs within the first 24 hours after retinal injury. Shortly thereafter, Müller glial cells upregulate genes typical of gliosis and then downregulate cyclin D3, in concert with an exit from mitosis. Mice lacking p27 Kip1 showed a constitutive form of reactive gliosis, which leads to retinal dysplasia and vascular abnormalities reminiscent of diabetic retinopathy. We conclude that p27 Kip1 regulates Müller glial cell proliferation during reactive gliosis.
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