NDLI: Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lagrèze, Wolf A. Schallner, Nils Van Oterendorp, Christian Sgouris, Stavros Biermann, Julia
Description	Country affiliation: Germany Author Affiliation: van Oterendorp C ( Department of Ophthalmology, Georg-August-University Hospital, Göttingen, Germany.)
Abstract	PURPOSE: Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. METHODS: Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (superior colliculus [SC] injection), axonal tyrosine kinase receptor (Trk) receptor inhibition with genistein, and acute axonal damage by optic nerve transection (ONT) were investigated at time points from 24 hours to 5 days. RESULTS: ERK5 and MEK5 were present in RGCs and glial cells. Phospho-ERK5 levels increased in retina and decreased in brain with age (n = 4; P = 0.039). Phosphorylation of ERK5 but not ERK1/2 was increased or decreased by SC injection of BDNF or genistein, respectively (BDNF at 48 hours [p-ERK5: P = 0.01; p-ERK1/2: P = 0.55, n = 8]; genistein at 48 hours [p-ERK5: P = 0.01; p-ERK1/2: P = 0.5, n = 5]). ONT showed a similar trend. BDNF stimulation at the RGC soma increased both p-ERK5 and p-ERK1/2 (P = 0.035 and P = 0.032, respectively; n = 6; at 48 hours). CONCLUSIONS: ERK5 is present in RGCs. Retina and brain p-ERK5 levels develop differently with age. The response of ERK5 but not ERK1/2 to BDNF stimulation or inhibition at the RGC axon ending indicates that retrograde neurotrophic signals in the rat optic nerve may be mediated by the ERK5 pathway.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	2
Volume Number	55
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2014-02-03
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Brain-derived Neurotrophic Factor Pharmacology Map Kinase Signaling System Physiology Mitogen-activated Protein Kinase 1 Metabolism Mitogen-activated Protein Kinase 3 Mitogen-activated Protein Kinase 7 Retinal Ganglion Cells Drug Effects Aging Animals Blotting, Western Brain Enzymology Intravitreal Injections Neuroglia Optic Nerve Injuries Phosphorylation Rats, Sprague-dawley Retina Superior Colliculi Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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