PMID- 21255129
OWN - NLM
STAT- MEDLINE
DCOM- 20110701
LR  - 20110309
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 33
IP  - 5
DP  - 2011 Mar
TI  - Involvement of endoplasmic reticulum stress on neuronal cell death in the lateral 
      geniculate nucleus in the monkey glaucoma model.
PG  - 843-55
LID - 10.1111/j.1460-9568.2010.07578.x [doi]
AB  - We investigated whether endoplasmic reticulum (ER) stress was involved in the 
      pathophysiological mechanisms underlying neuronal death of the lateral geniculate 
      nucleus (LGN) after intraocular pressure (IOP) elevation. Five cynomolgus 
      monkeys, four with a glaucomatous left eye after laser photocoagulation treatment 
      and one normal monkey, were studied. At 4, 11, 15 and 24 weeks after the laser 
      photocoagulation treatment, the numbers of LGN neurons and atrophy were 
      immunohistochemically evaluated using anti-parvalbumin-antibody, which was used 
      to specifically label relay neurons connecting to the visual cortex. In addition, 
      terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling 
      (TUNEL)-positive cells, polyubiquitin, and production of ER stress-related 
      proteins, such as the phosphorylation of eukaryotic initiation factor 2alpha 
      (p-eIF2alpha) and C/EBP-homologous protein (CHOP), were also measured using in situ 
      hybridization and immunostaining. Loss of neurons and/or neuronal atrophy in 
      layers 1, 4 and 6 of the LGN on the contralateral side were observed at 4-24 
      weeks after the laser photocoagulation treatment. Furthermore, the retinal input 
      from the high IOP eye projected to layers 2 (magnocellular layer), 3 and 5 
      (parvocellular layer) on the ipsilateral side. Neuronal damage was also confirmed 
      in these layers. In the LGN region, TUNEL-positive cells, polyubiquitin, p-eIF2alpha 
      and CHOP were also detected at 11-24 weeks after the laser photocoagulation 
      treatment. These findings indicate that ER stress may play a pivotal role in 
      neuronal death of the LGN after IOP elevation.
CI  - (c) 2011 The Authors. European Journal of Neuroscience (c) 2011 Federation of 
      European Neuroscience Societies and Blackwell Publishing Ltd.
FAU - Ito, Yasushi
AU  - Ito Y
AD  - Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu 
      Pharmaceutical University, 1-25-4 Daigaku-Nishi, Gifu 501-1196, Japan.
FAU - Shimazawa, Masamitsu
AU  - Shimazawa M
FAU - Inokuchi, Yuta
AU  - Inokuchi Y
FAU - Yamanaka, Hajime
AU  - Yamanaka H
FAU - Tsuruma, Kazuhiro
AU  - Tsuruma K
FAU - Imamura, Kazuyuki
AU  - Imamura K
FAU - Onoe, Hirotaka
AU  - Onoe H
FAU - Watanabe, Yasuyoshi
AU  - Watanabe Y
FAU - Aihara, Makoto
AU  - Aihara M
FAU - Araie, Makoto
AU  - Araie M
FAU - Hara, Hideaki
AU  - Hara H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110124
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 147336-12-7 (Transcription Factor CHOP)
SB  - IM
MH  - Animals
MH  - Cell Death/*physiology
MH  - *Disease Models, Animal
MH  - Endoplasmic Reticulum/*metabolism
MH  - *Geniculate Bodies/cytology/pathology/physiology
MH  - Glaucoma/pathology/*physiopathology
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Intraocular Pressure/physiology
MH  - Macaca fascicularis
MH  - Male
MH  - Neurons/cytology/*physiology
MH  - Optic Nerve/cytology/pathology/physiology
MH  - Retina/cytology/pathology/physiology
MH  - *Stress, Physiological
MH  - Transcription Factor CHOP/metabolism
EDAT- 2011/01/25 06:00
MHDA- 2011/07/02 06:00
CRDT- 2011/01/25 06:00
PHST- 2011/01/25 06:00 [entrez]
PHST- 2011/01/25 06:00 [pubmed]
PHST- 2011/07/02 06:00 [medline]
AID - 10.1111/j.1460-9568.2010.07578.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2011 Mar;33(5):843-55. doi: 10.1111/j.1460-9568.2010.07578.x. 
      Epub 2011 Jan 24.