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Intercellular junctions of hyperplastic retinal pigment epithelium.
Experientia
|July 15, 1986
Summary
In rats, retinal pigment epithelium (RPE) hyperplasia due to light or urethane damage prevents molecule passage. Intact tight junctions in hyperplastic RPE cells form a barrier, blocking substances from the sensory retina.
Area of Science:
- Ophthalmology
- Cell Biology
- Toxicology
Background:
- Retinopathies can cause damage to the retinal pigment epithelium (RPE).
- The RPE forms a critical barrier between the sensory retina and the choroid.
Purpose of the Study:
- To investigate the permeability barrier of hyperplastic RPE in induced rat retinopathies.
- To identify the cellular structures responsible for barrier function in these conditions.
Main Methods:
- Induction of retinopathy in rats using excess fluorescent light or urethane injection.
- Intravascular and intraocular injection of tracer molecules (horseradish peroxidase, lanthanum nitrate, microperoxidase).
- Examination of retinal tissue using electron microscopy.
Main Results:
- Focal hyperplasia of the RPE was observed in rats with induced retinopathies.
- Intravascular and intraocular tracers did not penetrate the sensory retina at hyperplastic RPE sites.
- Electron microscopy confirmed the presence of intact tight junctions in the hyperplastic RPE layer facing the sensory retina.
- Adherent junctions within the hyperplastic foci did not impede tracer passage.
Conclusions:
- Persistent intact tight junctions in hyperplastic RPE cells re-establish a functional barrier.
- This barrier prevents the passage of molecules into the sensory retina, potentially impacting retinal health.