Cargando…
An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy
In retinopathy of prematurity (ROP), the abnormal retinal neovascularization is often accompanied by retinal neuronal dysfunction. Here, a rat model of oxygen‐induced retinopathy (OIR), which mimics the ROP disease, was used to investigate changes in the expression of key mediators of autophagy and...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8581343/ https://www.ncbi.nlm.nih.gov/pubmed/34623024 http://dx.doi.org/10.1111/jcmm.16977 |
_version_ | 1784596786891980800 |
---|---|
author | Pesce, Noemi Anna Canovai, Alessio Plastino, Flavia Lardner, Emma Kvanta, Anders Cammalleri, Maurizio André, Helder Dal Monte, Massimo |
author_facet | Pesce, Noemi Anna Canovai, Alessio Plastino, Flavia Lardner, Emma Kvanta, Anders Cammalleri, Maurizio André, Helder Dal Monte, Massimo |
author_sort | Pesce, Noemi Anna |
collection | PubMed |
description | In retinopathy of prematurity (ROP), the abnormal retinal neovascularization is often accompanied by retinal neuronal dysfunction. Here, a rat model of oxygen‐induced retinopathy (OIR), which mimics the ROP disease, was used to investigate changes in the expression of key mediators of autophagy and markers of cell death in the rat retina. In addition, rats were treated from birth to postnatal day 14 and 18 with 3‐methyladenine (3‐MA), an inhibitor of autophagy. Immunoblot and immunofluorescence analysis demonstrated that autophagic mechanisms are dysregulated in the retina of OIR rats and indicated a possible correlation between autophagy and necroptosis, but not apoptosis. We found that 3‐MA acts predominantly by reducing autophagic and necroptotic markers in the OIR retinas, having no effects on apoptotic markers. However, 3‐MA does not ameliorate retinal function, which results compromised in this model. Taken together, these results revealed the crucial role of autophagy in retinal cells of OIR rats. Thus, inhibiting autophagy may be viewed as a putative strategy to counteract ROP. |
format | Online Article Text |
id | pubmed-8581343 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85813432021-11-17 An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy Pesce, Noemi Anna Canovai, Alessio Plastino, Flavia Lardner, Emma Kvanta, Anders Cammalleri, Maurizio André, Helder Dal Monte, Massimo J Cell Mol Med Original Articles In retinopathy of prematurity (ROP), the abnormal retinal neovascularization is often accompanied by retinal neuronal dysfunction. Here, a rat model of oxygen‐induced retinopathy (OIR), which mimics the ROP disease, was used to investigate changes in the expression of key mediators of autophagy and markers of cell death in the rat retina. In addition, rats were treated from birth to postnatal day 14 and 18 with 3‐methyladenine (3‐MA), an inhibitor of autophagy. Immunoblot and immunofluorescence analysis demonstrated that autophagic mechanisms are dysregulated in the retina of OIR rats and indicated a possible correlation between autophagy and necroptosis, but not apoptosis. We found that 3‐MA acts predominantly by reducing autophagic and necroptotic markers in the OIR retinas, having no effects on apoptotic markers. However, 3‐MA does not ameliorate retinal function, which results compromised in this model. Taken together, these results revealed the crucial role of autophagy in retinal cells of OIR rats. Thus, inhibiting autophagy may be viewed as a putative strategy to counteract ROP. John Wiley and Sons Inc. 2021-10-08 2021-11 /pmc/articles/PMC8581343/ /pubmed/34623024 http://dx.doi.org/10.1111/jcmm.16977 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Pesce, Noemi Anna Canovai, Alessio Plastino, Flavia Lardner, Emma Kvanta, Anders Cammalleri, Maurizio André, Helder Dal Monte, Massimo An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title | An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title_full | An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title_fullStr | An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title_full_unstemmed | An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title_short | An imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
title_sort | imbalance in autophagy contributes to retinal damage in a rat model of oxygen‐induced retinopathy |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8581343/ https://www.ncbi.nlm.nih.gov/pubmed/34623024 http://dx.doi.org/10.1111/jcmm.16977 |
work_keys_str_mv | AT pescenoemianna animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT canovaialessio animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT plastinoflavia animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT lardneremma animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT kvantaanders animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT cammallerimaurizio animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT andrehelder animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT dalmontemassimo animbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT pescenoemianna imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT canovaialessio imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT plastinoflavia imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT lardneremma imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT kvantaanders imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT cammallerimaurizio imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT andrehelder imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy AT dalmontemassimo imbalanceinautophagycontributestoretinaldamageinaratmodelofoxygeninducedretinopathy |