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Stephanie Thebault, Edith Arnold, Rodrigo d Meléndez García, David Arredondo, German d Baeza-Cruz, Juan d Riesgo-Escovar, Vincent Goffin, Carmen Clapp; Prolactin contributes to the regulation of retinal pigment epithelial cell survival and monolayer resistance. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1883.
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We recently showed that the hormone prolactin (PRL) acts as an endogenous retinal trophic factor able to limit retinal degeneration. In addition to regulating glial-neuronal cell interactions in the retina, we postulated thatPRL targets retinal pigment epithelial (RPE) cells.
The presence of PRL receptor in the RPE of male albino rats was determined by in situ hybridization and immunochemistry, and in human ARPE-19 cell cultures by Western blot. The viability of ARPE-19 cell cultures was examined by MTT assay, and ARPE-19 cell monolayers were evaluated for transepithelial electrical resistance. A competitive PRL receptor antagonist was used to ensure the specificity of recombinant human PRL actions.
RPE in transverse sections of rat retinas was positive for PRL receptor mRNA and protein. PRL receptor was also detected in flat mounts of rat RPE and in ARPE-19 cell monolayers. A 48-hour PRL treatment increased the viability of ARPE-19 cell cultures in a dose-dependent manner, with a maximal effect dose of 100 pM (2.3 ng/ml). The PRL receptor antagonist increasingly reduced ARPE-19 cell viability at 10 nM, 100 nM and 1 µM. The effect of 10 nM PRL receptor antagonist was prevented by adding 100 pM rhPRL. Moreover, PRL induced a transient increase in the resistance of ARPE-19 monolayers that peaked at 30 minutes.
These findings show that the PRL receptor is present in the RPE, and that the stimulation of PRL signaling may help to regulate RPE permeability and survival.
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