Glucocorticoid and progesterone mechanisms in photoreceptor survival

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Glucocorticoid and progesterone mechanisms in photoreceptor survival

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dc.contributor.author Marquioni-Ramella, Melisa.
dc.contributor.author Cubilla, Marisa.
dc.contributor.author Bermúdez, Vicente.
dc.contributor.author Tate, Pablo.
dc.contributor.author Marazita, Mariela.
dc.contributor.author Suburo, Angela.
dc.date.accessioned 2020-10-01T20:53:42Z
dc.date.available 2020-10-01T20:53:42Z
dc.date.issued 2020-01-01
dc.identifier.citation Exp Eye Res . 2020 Jan;190:107854. en_US
dc.identifier.issn 0014-4835
dc.identifier.uri https://riu.austral.edu.ar/handle/123456789/970
dc.description Full Text https://www.sciencedirect.com/science/article/pii/S0014483519304427?via%3Dihub en_US
dc.description.abstract Abstract Death of retinal photoreceptors is the basis of prevalent blinding diseases. Since steroids might have a therapeutic role in retinal degenerations, we compared the protective effects of dexamethasone and progesterone on photoreceptor death induced by mifepristone and light exposure. Therefore, we studied the effective protection doses for each steroid in the two models. In addition, we analyzed changes in the levels of pro- and antiapoptotic molecules, glucocorticoid receptors α and β (GRα and GRβ), and rhodopsin under conditions of successful protection and photoreceptor survival. Mifepristone and light exposure selectively damaged photoreceptors. In light exposed retinas, photoreceptors mainly disappeared in the dorsotemporal region, while mifepristone produced a uniform damage. Dexamethasone and progesterone, at the same dose of 4 mg/kg/day for 2 days, preserved over 88% photoreceptor nuclei in both models. Assessment of cell death regulators showed that, in control retinas, both steroids activated BCL-XL, a prosurvival molecule, and decreased BID, a proapoptotic regulator. After steroid treatment of damaged retinas, BCL-XL, BCL2 and BAX showed characteristic patterns depending on the use of dexamethasone or progesterone on mifepristone or light exposed retinas. By contrast, BID decreased with any injury-steroid combination. Changes in GRα or GRβ levels did not correlate with survival but were consistent with a mechanism of ligand induced downregulation of receptor expression. GRβ might be upregulated by progesterone. Both dexamethasone and progesterone increased retinal rhodopsin stores, suggesting a link between photoreceptor protection and transduction pathways. Results show that dexamethasone and progesterone induced comparable but not identical protection responses in each model. en_US
dc.language.iso en en_US
dc.publisher Elsevier B.V. ScienceDirect en_US
dc.subject Apoptosis en_US
dc.subject Dexamethasone en_US
dc.subject Glucocorticoid receptor en_US
dc.subject Light exposure en_US
dc.subject Mifepristone en_US
dc.title Glucocorticoid and progesterone mechanisms in photoreceptor survival en_US
dc.type Article en_US


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