EMAP cytokine expression in developing retinas of normal and retinal degeneration (rd) mutant mice

Citation
Sh. Liu et al., EMAP cytokine expression in developing retinas of normal and retinal degeneration (rd) mutant mice, J NEUROIMM, 114(1-2), 2001, pp. 28-34
Citations number
22
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
114
Issue
1-2
Year of publication
2001
Pages
28 - 34
Database
ISI
SICI code
0165-5728(20010301)114:1-2<28:ECEIDR>2.0.ZU;2-U
Abstract
Endothelial-monocyte-activating polypeptide (EMAP) is a proinflammatory cyt okine and a mediator of programmed endothelial cell death. To gain insight into its possible functions during retinal development and degeneration, th e cellular distribution of EMAP protein was compared in control and retinal degeneration (rd) mice. EMAP immunoreactivity was confined to the ganglion cell layer (GCL) and the inner nuclear layer (INL). There were significant differences in the intensity of EMAP labeling in the GCL and the INL when comparing control and rd mouse retinas. Rd retinas contain much more EMAP i mmunoreactivity in the GCL and the INL than the control retinas at postnata l day 14, which is the time point immediately after the onset of the degene ration of the rd retina. Histopathologic examination showed no significant abnormalities in the GCL and INL in the rd mouse, despite a great degree of photoreceptor cell death from P12 to P18. Light and electron microscopic s tudies immunolocalize EMAP protein to the cytoplasm of retinal ganglion cel ls, amacrine cells, and horizontal cells. The data suggests that EMAP is sy nthesized and accumulated as an intracellular precursor protein that has a functional role in translation and protein synthesis as a cofactor for tRNA synthetase. The increased expression of EMAP precursor levels in rd mouse retina may reflect the enhanced rate of translation and protein synthesis i n the production of endogenous factors that promote survival in the GCL and INL. (C) 2001 Published by Elsevier Science B.V.