Presence of mitogen-activated protein kinase in retinal Müller cells and its neuroprotective effect ischemia-reperfusion injury

Hiroshi Akiyama; Toru Nakazawa; Masahiko Shimura; Hiroshi Tomita; Makoto Tamai

doi:10.1097/00001756-200211150-00022

Presence of mitogen-activated protein kinase in retinal Müller cells and its neuroprotective effect ischemia-reperfusion injury

Hiroshi Akiyama, Toru Nakazawa, Masahiko Shimura, Hiroshi Tomita, Makoto Tamai

MED - Medical Sciences

Research output: Contribution to journal › Article › peer-review

38 Citations (Scopus)

Abstract

The purpose of this study was to determine whether the mitogen-activated protein kinase (MAPK) signaling pathway in the retina plays a neuroprotective role against ischemia-reperfusion injury. Western blot analysis showed that the MAPK activity was markedly increased within an hour after ischemia-reperfusion and subsequently decreased. Immunohistochemical studies revealed that MAPK was expressed mainly in the retinal Müller cells (RMCs). Pre-ischemic intravitreal administration of a MAPK inhibitor, U0126, increased the number of ganglion cell deaths induced by ischemia-reperfusion injury. We conclude that the MAPK activated in the RMCs protects ganglion cells against the ischemia-reperfusion injury through glia-neuronal interaction.

Original language	English
Pages (from-to)	2103-2107
Number of pages	5
Journal	NeuroReport
Volume	13
Issue number	16
DOIs	https://doi.org/10.1097/00001756-200211150-00022
Publication status	Published - 2002 Nov 15

Keywords

Ischemia-reperfusion
Neuroprotection
Retinal Müller cells
Retinal ganglion cell

ASJC Scopus subject areas

Neuroscience(all)

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abstract = "The purpose of this study was to determine whether the mitogen-activated protein kinase (MAPK) signaling pathway in the retina plays a neuroprotective role against ischemia-reperfusion injury. Western blot analysis showed that the MAPK activity was markedly increased within an hour after ischemia-reperfusion and subsequently decreased. Immunohistochemical studies revealed that MAPK was expressed mainly in the retinal M{\"u}ller cells (RMCs). Pre-ischemic intravitreal administration of a MAPK inhibitor, U0126, increased the number of ganglion cell deaths induced by ischemia-reperfusion injury. We conclude that the MAPK activated in the RMCs protects ganglion cells against the ischemia-reperfusion injury through glia-neuronal interaction.",

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AU - Tomita, Hiroshi

AU - Tamai, Makoto

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N2 - The purpose of this study was to determine whether the mitogen-activated protein kinase (MAPK) signaling pathway in the retina plays a neuroprotective role against ischemia-reperfusion injury. Western blot analysis showed that the MAPK activity was markedly increased within an hour after ischemia-reperfusion and subsequently decreased. Immunohistochemical studies revealed that MAPK was expressed mainly in the retinal Müller cells (RMCs). Pre-ischemic intravitreal administration of a MAPK inhibitor, U0126, increased the number of ganglion cell deaths induced by ischemia-reperfusion injury. We conclude that the MAPK activated in the RMCs protects ganglion cells against the ischemia-reperfusion injury through glia-neuronal interaction.

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