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e experiments, Li and colleagues identified cone outer segments by peanut agglutinin labeling or by antibodies against cone opsins. Furthermore, antibodies against cone arrestin were employed to determine the cell bodies of cone photoreceptors. Loss of COS, an early DBeQ sign of cone degeneration, was detected as early as PD12, at the peak of rod degeneration. The loss of COS was not evenly distributed. Rather, DBeQ it was concentrated in several small patches that were negatively stained for PNA. The PNA negative areas expanded with age, indicating progressive loss of COS. Intravitreal injection of recombinant CNTF protein substantially changed the PNA negative areas. They became considerably smaller and in numerous instances entirely resolved. The reappearance of PNA staining within the prior PNA negative areas suggests regeneration of COS.
To prove that CNTF treatment induces regeneration of COS, the investigators compared the COS densities before and soon after CNTF treatment. They demonstrated that COS density was greater in CNTF treated retina than before the treatment, confirming that CNTF treatment did promote regeneration of COS. PluriSln 1 Given that loss of COS is an early sign of cone degeneration, regeneration of COS could be deemed as reversal in the degenerative approach. This result indicates that CNTF treatment may not only slow or stop degeneration, but may well also reverse the degeneration approach. Given that COS is part of the functional organelles of cone photoreceptors for light detection, the regeneration of COS could translate into functional improvement of cones.
In another experiment, significant long term protection of cone cells and cone ERG were achieved by using CNTF secreting implants for sustained delivery of CNTF towards the retina of S334ter rats. 6. 2. Protection of cones in Human musculoskeletal system human by CNTF As already described, the very first indication of a neurotrophic effect of CNTF on cones came from a small open label clinical trial of CNTF secreting implants in individuals with advanced RP. Though the trial objective was to figure out the safety in the CNTF implants along with the surgical procedure, the results showed that three individuals experienced an increase of 10 15 letters over baseline in visual acuity whereas no increase was observed within the untreated fellow eyes among the seven study eyes that could be tracked for visual acuity.
The improvement of visual acuity is likely to have resulted from the improvement of cone function, because visual acuity tests the function in the fovea, which has only cones, and in individuals with advanced RP, just about all rod photoreceptors have degenerated. PluriSln 1 The protective effect of CNTF on cone photoreceptors was objectively demonstrated in human individuals working with a effective imaging technology called the adaptive optics scanning laser ophthalmoscopy. Talcott and colleagues observed cones in three individuals over a 2 year period and identified a progressive cone density decreased in sham treated eyes. On the other hand, the cone density remained stable in CNTF treated eyes. Furthermore, a recent clinical trial of CNTF secreting implants in individuals with geographic atrophy showed a stabilization of visual acuity in eyes treated with high dose CNTF secreting implants.
Together, these findings indicate that CNTF is neuroprotective for cone photoreceptors. 6. 3. Restoration of cone function in dogs with CNGB3 mutations by CNTF Kom romy and colleagues DBeQ lately identified that a single intravitreal injection of recombinant CNTF protein in adult dogs with CNGB3 mutations, which causes day blindness in dogs, induced a transient restoration of cone function and vision. The cone ERGs became detectable for up to 4 weeks soon after injection. The treated animals also showed improved performance in navigating an obstacle course in bright light, indicating restoration of cone vision. There was additionally a transient decrease in rod ERG, which is consistent using the prior findings in rat and mice.
There's no functional B subunit in the cone cyclic nucleotide gated channel in CNGB3 dogs along with the mechanism in the restored cone function is unknown. The transient PluriSln 1 nature of these changes DBeQ is likely because of the clearance in the injected CNTF protein. 7. CNTF and retinal ganglion cells 7. 1. Neuroprotection CNTF serves a neurotrophic function for RGCs. A single injection of CNTF protein into PluriSln 1 the vitreous considerably protected RGCs in an optic nerve axotomy rat model, whereas brain derived neurotrophic factor did not. RGC protection by CNTF was also noticed in nitric oxide induced cell death. CNTF treatment 2 days prior to injection in the nitric oxide donor considerably protected RGCs from cell death. In culture, CNTF promoted the survival of purified rat RGCs within the presence of forskolin. CNTF gene transfer by way of Ad vectors also protects retinal ganglion cells from degeneration. RGC density within the eyes treated with intravitreal Ad CNTF 1 2 hours soon after optic nerve axotomy was considerably higher than within the controls when examined 14 days later. Equivalent protection