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MT Perez, A Aspberg, J Lee; Tenascin-R Accumulation in Association With the Retinal Vasculature in RCS Rats . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3483.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: As photoreceptor cell (PC) loss progresses, secondary pathological changes are observed both in animal models and in RP patients. The changes, involving glial cells, inner retinal neuronal cells, and the vasculature, are likely to require alterations in the structure of the extracellular matrix (ECM). Members of the tenascin family of ECM glycoproteins have been implicated in processes that accompany neuronal cell loss. We have therefore compared here the distribution of tenascin-R in normal retinas and in retinas from animals exhibiting PC loss, in order to determine whether its distribution can be correlated with any of the pathological changes observed. Methods: Retinas from developing and adult normal rats, dystrophic RCS rats, and transgenic rhodopsin mutant rats (P23H-line 1; S334ter-line 4) were processed for immunohistochemistry using a polyclonal antibody against recombinant rat tenascin-R produced in 293-EBNA cells. Results: In normal rats, tenascin-R immunoreactivity was found to be accumulated at embryonic day 18 in the developing inner plexiform layer (IPL) and pericellularly in the rest of the retina. At postnatal day 5 (P5), defined labeling was seen in association with horizontal cells, in the outer plexiform layer (OPL), in three bands in the IPL, and in the nerve fiber layer. No differences were noted in older specimens (P5-P60) in the distribution but in the intensity of the labeling which appeared to increase between P5 and P36. The same observations were made in retinas derived from young P23H and S334ter rats. At P60 and onwards (P60-P200), however, labeling in the OPL of P23H rats became increasingly uneven, and was generally weaker in the IPL. The same was observed in S334ter rats from P100-P200 and in RCS rats from P60-P300. An abnormal accumulation was however seen around superficial vessels and RPE-associated vessels in RCS rats from P45 and onwards. Conclusion: The reduced staining seen in the plexiform layers may simply reflect the loss of neuronal components in the aging dystrophic retinas. On the other hand, the enhanced expression seen in RCS rat retinas is more likely to correlate with the striking vascular changes (vascular atrophy and neovascularization) observed in this animal model, suggesting that tenascin-R may, by interactions with other ECM molecules, play a role in these processes. Little is known about the vasculature in aging P23H and S334ter rats, but our observations suggest that vascular alterations in these animals are either considerably slower or involve other types of interactions.
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