Nestin Expression in the Adult Mouse Retina with Pharmaceutically Induced Retinal Degeneration
- Authors
- Moon, Chan Hee; Cho, Heeyoon; Kim, Yoon Kyung; Park, Tae Kwann
- Issue Date
- Feb-2017
- Publisher
- 대한의학회
- Keywords
- Nestin; N-methyl-N-nitrosourea (MNU); Retinal Degeneration; Mouse
- Citation
- Journal of Korean Medical Science, v.32, no.2, pp 343 - 351
- Pages
- 9
- Journal Title
- Journal of Korean Medical Science
- Volume
- 32
- Number
- 2
- Start Page
- 343
- End Page
- 351
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/7814
- DOI
- 10.3346/jkms.2017.32.2.343
- ISSN
- 1011-8934
1598-6357
- Abstract
- The present study investigated the temporal pattern and cellular localization of nestin in the adult mouse retina with pharmaceutically induced retinal degeneration using N-methyl-N-nitrosourea (MNU). After a single intraperitoneal injection of MNU in 8-weekold C57BL/6 mice, the animals were sacrificed at 1, 3, 5, 7, and 21 days (n=6, in each stage). The eyes were examined by means of immunohistochemical tests using nestin, ionized calcium-binding adaptor molecule (Iba-1), CD11b, F4/80, and glial fibrillary acidic protein (GFAP). Western blot analysis and manual cell counting were performed for quantification. Nestin expression was increased after MNU administration. Nestin+/Iba-1+ cells were migrated into outer nuclear layer (ONL) and peaked at day 3 post injection (PI). Nestin+/CD11b+ cells were also mainly identified in ONL at day 3 PI and peaked at day 5. Nestin+/F4/80+ cells were shown in the subretinal space and peaked at day 3 PI. Nestin+/GFAP+ cells were distinctly increased at day 1 PI and peaked at day 5 PI. The up-regulation of nestin expression after MNU administration in adult mouse retinal microglia, and monocyte/macrophage suggests that when retinal degeneration progresses, these cells may revert to a more developmentally immature state. Muller cells also showed reactive gliosis and differentiational changes.
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Collections - College of Medicine > Department of Ophthalmology > 1. Journal Articles
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