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Toru Kurokawa, Naomichi Katai, Hiroto Shibuki, Sachiko Kuroiwa, Yasuo Kurimoto, Chikao Nakayama, Nagahisa Yoshimura; BDNF Diminishes Caspase-2 but Not c-Jun Immunoreactivity of Neurons in Retinal Ganglion Cell Layer after Transient Ischemia. Invest. Ophthalmol. Vis. Sci. 1999;40(12):3006-3011.
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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
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 μg) 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
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.
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