| First Author | Jones SE | Year | 1998 |
| Journal | Neuroreport | Volume | 9 |
| Issue | 18 | Pages | 4161-5 |
| PubMed ID | 9926867 | Mgi Jnum | J:52955 |
| Mgi Id | MGI:1330697 | Doi | 10.1097/00001756-199812210-00030 |
| Citation | Jones SE, et al. (1998) Expression of alphaB-crystallin in a mouse model of inherited retinal degeneration. Neuroreport 9(18):4161-5 |
| abstractText | alpha beta-CRYSTALLIN, Which is abundantly expressed in the lens but also in a diversity of other tissues, functions as a stress-inducible molecular chaperone and is increased in brain neurodegenerative diseases. We compared retinal alpha beta-crystallin expression in a model of inherited retinal degeneration, the rd mouse, and controls. Northern and in situ hybridization analysis showed alpha beta-crystallin mRNA to have an altered spatio-temporal pattern with increased levels localized to glial cells in the degenerative state. Immunocytochemistry confirmed increased expression at Muller cells and astrocytes, together With transiently increased localization to the degenerating photoreceptors. These findings suggest that increased alpha beta-crystallin expression is associated with glial cell reaction to neuronal damage in the retina, and may comprise part of the retina's overall defensive response to the stress of apoptotic photoreceptor cell death. (C) 1998 Lippincott Williams & Wilkins. |
