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Journal of Neuroscience, Vol 12, 3554-3567, Copyright © 1992 by Society for Neuroscience
Basic fibroblast growth factor and local injury protect photoreceptors from light damage in the rat
EG Faktorovich, RH Steinberg, D Yasumura, MT Matthes and MM LaVail
Department of Ophthalmology, University of California, San Francisco 94143-0730.
Injection of basic fibroblast growth factor (bFGF) into the eye,
intravitreally or subretinally, delays photoreceptor degeneration in
inherited retinal dystrophy in the rat, as does local injury to the retina
(Faktorovich et al., 1990). To determine whether this heparin- binding
peptide or local injury is effective in any other form of photoreceptor
degeneration, we examined their protective roles in light damage. Albino
rats of the F344 strain were exposed to 1 or 2 weeks of constant
fluorescent light (115-200 footcandles), either with or without 1
microliter of bFGF solution (1150 ng/microliters in PBS) injected
intravitreally or subretinally 2 d before the start of light exposure.
Uninjected and intravitreally PBS-injected controls showed the loss of a
majority of photoreceptor nuclei and the loss of most inner and outer
segments after 1 week of light exposure, while intravitreal injection of
bFGF resulted in significant photoreceptor rescue. The outer nuclear layer
in bFGF-injected eyes was two to three times thicker than in controls, and
the inner and outer segments showed a much greater degree of integrity.
Following recovery in cyclic light for 10 d after 1 week of constant light
exposure, bFGF-injected eyes showed much greater regeneration of
photoreceptor inner and outer segments than did the controls. bFGF also
increased the incidence of presumptive macrophages, located predominantly
in the inner retina, but the evidence suggests they are not directly
involved in photoreceptor rescue. Subretinal injection of bFGF resulted in
photoreceptor rescue throughout most of the superior hemisphere in which
the injection was made, with rescue extending into the inferior hemisphere
in many of the eyes. Remarkably, the insertion of a dry needle or injection
of PBS into the subretinal space also resulted in widespread photoreceptor
rescue, extending through 70% or more of the superior hemisphere, and
sometimes into the inferior hemispheres. This implicates the release and
widespread diffusion of some endogenous survival-promoting factor from the
site of injury in the retina. Our findings indicate that the photoreceptor
rescue activity of bFGF is not restricted to inherited retinal dystrophy in
the rat, and that light damage is an excellent model for studying the
cellular site(s), kinetics, and molecular mechanisms of both the normal
function of bFGF and its survival- promoting activity. Moreover, the
injury-related rescue suggests that survival-promoting factors are readily
available to provide a protective role in case of injury to the retina,
presumably comparable to those that mediate the "conditioning lesion"
effect in other neuronal systems.
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[Abstract]
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2724 - 2734.
[Abstract]
[Full Text]
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Light Treatment Enhances Photoreceptor Survival in Dystrophic Retinas of Royal College of Surgeons Rats
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40(10):
2383 - 2390.
[Abstract]
[Full Text]
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August 1, 1999;
40(9):
2088 - 2099.
[Abstract]
[Full Text]
[PDF]
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82(1):
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[Abstract]
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