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Xiaoman Li, Michael H. Elliott; Erk Phosphorylation Is Negatively Regulated By Caveolin-1 In Müller Glial Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3550.
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© ARVO (1962-2015); The Authors (2016-present)
Caveolin-1 (Cav-1) is an integral membrane protein reportedly involved in many cellular events such as membrane transport, lipid homeostasis and cell signaling. Clear evidence is accumulating that Cav-1 has cell context-specific functions. In retina, Cav-1 is highly expressed in Müller glia but its function in these cells is unknown. When retinas are under stress, Müller cells undergo an incompletely understood process of gliosis characterized by GFAP expression and involving activation of the MAPK/ERK pathway. As Cav-1 may regulate the MAPK/ERK pathway, we asked if Cav-1 might regulate ERK phosphorylation in Müller cells.
The spontaneously immortalized Müller cell line, MIO-M1, was maintained in DMEM medium containing 10% FBS and 1% penicillin/streptomycin at 37 °C with 5% CO2. Cav-1 expression was silenced using validated siRNA oligonucleotides. ERK phosphorylation was assessed by Western blot and confocal microscopy. In some experiments, MIO-M1 cells were subjected to hyperosmotic or oxidative stress using sorbitol or hydrogen peroxide, respectively. Retinal sections from Cav-1 null mice were examined by immunohistochemisty and confocal microscopy.
After transient Cav-1 knockdown, ERK phosphorylation was increased in MIO-M1 cells as detected by both Western blotting and confocal microscopy. Surprisingly, this enhanced phosphorylation was blunted when cells were exposed to hyperosmotic and oxidative stresses. In addition, Müller cells in Cav-1 null retinas exhibited ERK hyperphosphorylation, in vivo, as compared to control.
Cav-1 negatively regulates ERK phosphorylation in Müller cells in culture and in situ suggesting that Cav-1 may play an important role in Müller cell proliferation and possibly gliosis.
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