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The Neuroprotective Effect of the Adiponectin Receptor Agonist AdipoRon on Glutamate-Induced Cell Death in Rat Primary Retinal Ganglion Cells.

Authors
  • Uchida, Takatoshi1, 2
  • Ueta, Takashi1, 3
  • Honjo, Megumi1
  • Aihara, Makoto1
  • 1 Department of Ophthalmology, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan. , (Japan)
  • 2 Senju Laboratory of Ocular Science, Senju Pharmaceutical Co., Ltd., Kobe, Japan. , (Japan)
  • 3 Department of Ophthalmology, Center Hospital of the National Center for Global Health and Medicine, Tokyo, Japan. , (Japan)
Type
Published Article
Journal
Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
Publication Date
Dec 01, 2019
Volume
35
Issue
10
Pages
535–541
Identifiers
DOI: 10.1089/jop.2018.0152
PMID: 31460821
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Purpose: To determine whether the adiponectin receptor (AdipoR) agonist AdipoRon inhibits glutamate-induced neuronal cell death and to investigate the neuroprotective mechanism of AdipoRon in rat primary retinal ganglion cells (RGCs). Methods: The expression pattern of AdipoR1 and AdipoR2 in rat retina and primary RGCs was examined by immunostaining. The neuroprotective effect of AdipoRon on glutamate-induced cell death was evaluated in rat primary RGCs. Cellular levels of reactive oxygen species (ROS) were also measured. Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), estrogen-related receptor-α (Esrra), mitochondrial transcription factor A (TFAM), peroxisome proliferator-activated receptor α (PPARα), and catalase mRNA levels were examined. Results: The expression of AdipoR1 and AdipoR2 was confirmed in rat retina and primary RGCs. AdipoRon significantly increased the survival rate of glutamate-induced cell death and decreased ROS production. Additionally, the mRNA levels of PGC-1α, Esrra, and TFAM were upregulated by AdipoRon. Conclusions: These results suggest that AdipoRon has a neuroprotective effect by inhibiting ROS production via upregulation of PGC-1α, Esrra, and TFAM against glutamate-induced RGC death.

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