| First Author | Dyer MA | Year | 2000 |
| Journal | Nat Neurosci | Volume | 3 |
| Issue | 9 | Pages | 873-80 |
| PubMed ID | 10966617 | Mgi Jnum | J:109384 |
| Mgi Id | MGI:3628856 | Doi | 10.1038/78774 |
| Citation | Dyer MA, et al. (2000) Control of Muller glial cell proliferation and activation following retinal injury. Nat Neurosci 3(9):873-80 |
| abstractText | Muller glial cells are the major support cell for neurons in the vertebrate retina. Following neuronal damage, Muller cells undergo reactive gliosis, which is characterized by proliferation and changes in gene expression. We have found that downregulation of the tumor supressor protein p27Kip1 and re-entry into the cell cycle occurs within the first 24 hours after retinal injury. Shortly thereafter, Muller glial cells upregulate genes typical of gliosis and then downregulate cyclin D3, in concert with an exit from mitosis. Mice lacking p27Kip1 showed a constitutive form of reactive gliosis, which leads to retinal dysplasia and vascular abnormalities reminiscent of diabetic retinopathy. We conclude that p27Kip1 regulates Muller glial cell proliferation during reactive gliosis. |
