PMID- 10549664
OWN - NLM
STAT- MEDLINE
DCOM- 19991108
LR  - 20061115
IS  - 0146-0404 (Print)
IS  - 0146-0404 (Linking)
VI  - 40
IP  - 12
DP  - 1999 Nov
TI  - BDNF diminishes caspase-2 but not c-Jun immunoreactivity of neurons in retinal 
      ganglion cell layer after transient ischemia.
PG  - 3006-11
AB  - PURPOSE: Retinal ischemia-reperfusion injury induces apoptosis of retinal 
      neurons. The purpose of this study was to examine the association of c-Jun, 
      caspase-1, -2, and -3 immunoreactivities and neuronal apoptosis in the retinal 
      ganglion cell layer (GCL) and to study the effects of intravitreal brain-derived 
      neurotrophic factor (BDNF) on the expression of these gene products in a rat 
      model of retinal ischemia-reperfusion injury. METHODS: After 60 minutes of 
      ischemia, eyes were enucleated after 3, 6, 12, 24, and 168 hours of reperfusion. 
      The numbers of c-Jun-, caspase-1-, caspase-2-, caspase-3, and TdT-dUTP terminal 
      nick-end labeling (TUNEL)-positive cells in the GCL were counted. Recombinant 
      human BDNF (5 microg) or vehicle was injected intravitreally immediately after 
      reperfusion. At 6, 24, and 168 hours, the numbers of immunoreactive cells in 
      BDNF- and vehicle-treated groups were compared. RESULTS: Expression of c-Jun and 
      caspase-2 was found in dying cells in flat-mounted retinas. The numbers of 
      caspase-1- and caspase-3-positive cells were fewer than c-Jun- or 
      caspase-2-positive cells. Cell death in the retinal GCL was suppressed by an 
      intravitreal injection of BDNF. The numbers of TUNEL- and caspase-2-positive 
      cells were lower in the BDNF-treated group at 6 hours after reperfusion (P<0.01). 
      The number of c-Jun-positive cells in the treated retinas was not altered by the 
      treatment. CONCLUSIONS: Expression of c-Jun and caspase-2 is associated with 
      neuronal cell apoptosis in the GCL. Suppression of caspase-2 expression may 
      explain the neuroprotective effects of BDNF.
FAU - Kurokawa, T
AU  - Kurokawa T
AD  - Department of Ophthalmology, Shinshu University School of Medicine, Matsumoto, 
      Japan.
FAU - Katai, N
AU  - Katai N
FAU - Shibuki, H
AU  - Shibuki H
FAU - Kuroiwa, S
AU  - Kuroiwa S
FAU - Kurimoto, Y
AU  - Kurimoto Y
FAU - Nakayama, C
AU  - Nakayama C
FAU - Yoshimura, N
AU  - Yoshimura N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (Recombinant Proteins)
RN  - EC 3.4.22.- (Caspase 2)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Caspase 2
MH  - Caspases/*metabolism
MH  - Cell Count
MH  - Cell Survival/drug effects
MH  - Female
MH  - Fluorescent Antibody Technique, Indirect
MH  - In Situ Nick-End Labeling
MH  - Neurons, Afferent/*drug effects/metabolism/pathology
MH  - Proto-Oncogene Proteins c-jun/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Recombinant Proteins/pharmacology
MH  - Reperfusion Injury/metabolism/pathology/*prevention & control
MH  - Retinal Ganglion Cells/*drug effects/metabolism/pathology
MH  - Retinal Vessels
EDAT- 1999/11/05 00:00
MHDA- 1999/11/05 00:01
CRDT- 1999/11/05 00:00
PHST- 1999/11/05 00:00 [pubmed]
PHST- 1999/11/05 00:01 [medline]
PHST- 1999/11/05 00:00 [entrez]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 1999 Nov;40(12):3006-11.