期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 198, 期 1-2, 页码 56-61出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2008.04.014
关键词
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资金
- INSERM
- ANR [AO5088DS, AO5120DD]
- European Grant [LSHB-CT-2005-518167]
- PNR vision [AO6004SP]
- Fondation NRJ-Institut de France
- Assistance Publique-Hopitaux de Paris
We recently showed that subretinal CX3CR1-dependent microglial cell (MC) accumulation may lead to age-related macular degeneration. The fate of MC after engulfing retinal debris is poorly understood. Severe photoreceptor degeneration was observed 40days after exposure to bright light in CX3CR1-deficient but not control mice, and more MCS accumulated in the subretinal space of the former than the latter. To study the fate of subretinal MCs in CX3CR1 competent animals, we used a dystrophic rat model in which abundant subretinal MC accumulation is observed secondary to retinal degeneration. In dystrophic rats. MCs containing rhodopsin or rod outer segment (ROS) debris were found outside the outer retina at sites suggesting choroidal and ciliary egress. In conclusion. our data indicate that MC accumulation at injury sites is independent of CX3CR1 and precedes photoreceptor degeneration. The ectopic presence of rhodopsin-positive MCs suggests that CX3CR1 participates in MC egress from the outer retina. (C) 2008 Elsevier B.V. All rights reserved.
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