科研之友
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摘要
The Muller glial cells exhibit stem cell properties and express neuronal markers following experimentally induced retinal injury. However, it is not known whether Muller glia respond similarly to degenerative neuronal loss caused by genetic mutation. Here, we asked whether Muller cells dedifferentiate and express neuronal proteins in rd1 mouse, a naturally occurring mutant model of inherited retinal degeneration. Using immunohistochemistry and Western blotting, we studied expression patterns of glial fibrillary acidic protein (GFAP), nestin, rhodopsin, protein kinase C alpha (PKC alpha), beta-III-tubulin and recoverin in Muller glia. Reverse transcriptase-polymerase chain reaction (RT-PCR) was carried out to detect any rhodopsin mRNA in the rd1 mouse retina. We found that Muller cell processes in rd1 mouse hypertrophied and overexpressed GFAP as early as postnatal day (P)-14, features that were maintained throughout development and in the adult stage. Furthermore, Muller cells continued to express nestin, a progenitor cell marker, up to 6 months of age, raising the possibility that they remain undifferentiated for several months in rd1 mouse. We did not find nestin expression in Muller cells in 1-year-old rd1 mouse. Interestingly, Muller cell processes in rd1 mouse also expressed rhodopsin, a rod-specific protein. The rhodopsin expression in Muller cells was evident at P-21, and remained so up to at least 1 year of age. The expression of rhodopsin by Muller cells was further supported by our finding of the rhodopsin transcript in the 9-month-old rd1 mouse retina. We did not find the expression of PKC alpha, beta-III-tubulin or recoverin in Muller cells in adult rd1 mouse. These results suggested that Muller cells in rd1 mouse express proteins specific to retinal neurons that are the primary targets of the mutation in this mouse. Although the functional significance of rhodopsin expression by Muller cells is unclear, these results have implications for novel therapeutic strategies for retinal degeneration.
- 出版日期2012-12-6
