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V. T. Ciavatta, M. K. Kim, A. E. Faulkner, M. T. Pardue; Increased Expression of FGF2 After Implantation With a Microphotodiode Array in S334ter-3 Rats Despite the Absence of Retinal Preservation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):663.
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© ARVO (1962-2015); The Authors (2016-present)
Dystrophic RCS rats implanted with a subretinal microphotodiode array (MPA) show delayed photoreceptor death, temporary preservation of ERG b-waves (Pardue et al., 2005) and elevated FGF2 expression. The purpose of this work was to determine if these effects occur in implanted S334ter-3 rats.
Two week-old S334ter-3 rats were divided into four treatment groups such that one eye was unoperated (control) and the other eye was implanted with an inactive- or active device (Optobionics Corp.), sham operated, or unoperated. One week after surgery, retinal function was measured using dark-adapted ERGs and animals were sacrificed. Retinas were dissected for quantitative RT-PCR of FGF2.
One week after implantation, ERG b-wave amplitudes were indistinguishable across S334ter-3 treatment groups. However, quantitative RT-PCR indicated the ratio of FGF2 expression in operated eye to contralateral eye was three fold greater for implanted animals versus sham and control animals.
S334ter-3 rats undergo a rapid photoreceptor degeneration due to expression of an aberrant form of rhodopsin, whereas RCS rats undergo a slightly slower retinal degeneration due to expression of a mutated retinal pigment epithelium-specific receptor tyrosine kinase gene (Mertk). As anticipated from previous analyses of S334ter-3 rats (T.A. Walker et al., ARVO 2005, #5267), animals implanted with a subretinal MPA did not exhibit preservation of retinal function. However, FGF2 expression increased in implanted eyes. Since degeneration was not delayed in S334ter-3 rats despite increased FGF2 expression, the level of induction of this growth factor alone may not be sufficient to delay degeneration as observed in implanted RCS rats. Alternatively, degeneration in S334ter-3 rats may have progressed too rapidly to be amenable to FGF2 induction during the third postnatal week, and therefore, testing the MPA in slower retinal degeneration models is required.
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