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Published on: July 14, 2020
EMAP cytokine expression in developing retinas of normal and retinal degeneration (rd) mutant mice
S H Liu1, J D Gottsch, S A Vinores
1Wilmer Eye Institute, Johns Hopkins University School of Medicine, 467 Woods Building, Baltimore, MD 21205, USA. samliu@jhmi.edu
Abstract:
Endothelial-monocyte-activating polypeptide (EMAP) is a proinflammatory cytokine and a mediator of programmed endothelial cell death. To gain insight into its possible functions during retinal development and degeneration, the 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 immunoreactivity in the GCL and the INL than the control retinas at postnatal day 14, which is the time point immediately after the onset of the degeneration 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 studies immunolocalize EMAP protein to the cytoplasm of retinal ganglion cells, amacrine cells, and horizontal cells. The data suggests that EMAP is synthesized 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 in the production of endogenous factors that promote survival in the GCL and INL.
Insights
Endothelial-monocyte-activating polypeptide (EMAP) shows increased levels in degenerating mouse retinas, particularly in the ganglion cell layer. This suggests EMAP precursor protein may play a role in cellular survival during retinal degeneration.
Area of Science:
- Ophthalmology
- Neuroscience
- Cell Biology
Background:
- Endothelial-monocyte-activating polypeptide (EMAP) is a proinflammatory cytokine.
- EMAP is implicated in programmed endothelial cell death.
- Its role in retinal development and degeneration is not well understood.
Purpose of the Study:
- To investigate the cellular distribution and expression of EMAP protein in normal and degenerating mouse retinas.
- To understand the potential function of EMAP during retinal degeneration.
Main Methods:
- Immunohistochemistry and immunoelectron microscopy were used to localize EMAP protein in control and retinal degeneration (rd) mouse retinas.
- Comparison of EMAP immunoreactivity between control and rd retinas at postnatal day 14.
Main Results:
- EMAP immunoreactivity was localized to the ganglion cell layer (GCL) and inner nuclear layer (INL) in both control and rd retinas.
- Rd retinas exhibited significantly higher EMAP immunoreactivity in the GCL and INL compared to control retinas.
- EMAP protein was immunolocalized to the cytoplasm of retinal ganglion cells, amacrine cells, and horizontal cells.
Conclusions:
- EMAP is synthesized and accumulated as an intracellular precursor protein, potentially acting as a cofactor for tRNA synthetase in translation and protein synthesis.
- Elevated EMAP precursor levels in rd mouse retinas may indicate increased translation and protein synthesis to produce endogenous survival factors for the GCL and INL.

