| First Author | Hu Z | Year | 2016 |
| Journal | Cell Death Dis | Volume | 7 |
| Issue | 11 | Pages | e2468 |
| PubMed ID | 27831552 | Mgi Jnum | J:280222 |
| Mgi Id | MGI:6369122 | Doi | 10.1038/cddis.2016.363 |
| Citation | Hu Z, et al. (2016) Knockout of Ccr2 alleviates photoreceptor cell death in rodent retina exposed to chronic blue light. Cell Death Dis 7(11):e2468 |
| abstractText | Age-related macular degeneration (AMD), the leading cause of visual loss after the age of 60 years, is a degenerative retinal disease involving a variety of environmental and hereditary factors. Although it has been implicated that immune system is involved in the disease progression, the exact role that microglia has is still unclear. Here we demonstrated that knockout of Ccr2 gene could alleviate photoreceptor cell death in mice retinas exposed to chronic blue light. In Ccr2(-/-) mice, a damaged microglia recruitment was shown in retina and this could protect the visual function in electroretinogram and alleviate the photoreceptor apoptosis, which thus helped attenuate the blue light-induced retinopathy. We further found an increased co-location of NLRP3, Iba-1, and IL-1beta in fluorescence and a concomitant increased protein expression of NLRP3, caspase-1, and IL-1beta in western blotting in chronic blue light-induced retinopathy. Moreover, the activation of microglia and their cellular NLRP3 inflammasomes occurred as an earlier step before the structural and functional damage of the mice retinas, which collectively supported that microglial NLRP3 inflammasome might be the key to the chronic blue light-induced retinopathy. |
