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

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.

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