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|Title:||Müller glial cells express nestin coupled with glial fibrillary acidic protein in experimentally induced glaucoma in the rat retina|
Müller glial cells
|Citation:||Xue, L.P., Cao, Q., Ling, E.-A., Hu, S., Lu, J., Ding, P. (2006). Müller glial cells express nestin coupled with glial fibrillary acidic protein in experimentally induced glaucoma in the rat retina. Neuroscience 139 (2) : 723-732. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neuroscience.2005.12.032|
|Abstract:||This study was aimed to investigate reactive changes of Müller glial cells in rats subjected to experimentally induced glaucoma. In the latter, it is well documented that elevated intraocular pressure leads to the loss of ganglion cells as confirmed in this study. The present results have shown that Müller glial cells as well as astrocytes closely associated with the ganglion cells reacted vigorously to increased intraocular pressure as manifested by the induced and upregulated expression of nestin and glial fibrillar acidic protein. A major finding in glaucomatous rats was the induced expression of nestin together with glial fibrillar acidic protein with the rise of the intraocular pressure beginning at 2 h. The marked nestin expression appeared to be most intense at 1 week after operation and was sustained at 3 weeks. Induced nestin expression in Müller glial cells was demonstrated unequivocally in whole-mount preparation of the retina. In the same tissue preparation, nestin expression was also detected in some astrocytes. Western blotting analysis confirmed a marked increase in expression of nestin and glial fibrillar acidic protein. Present results suggest that nestin as well as glial fibrillar acidic protein is a useful biomarker for retina injury. The induced expression of these intermediate filament proteins in Müller glial cells especially at their end-feet and also in some astrocytes adjoining the neuronal injury suggests a potential neuroprotective mechanism in response to acute rise in intraocular pressure resulting in neuronal degeneration. © 2005 IBRO.|
|Appears in Collections:||Staff Publications|
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