UVA induces retinal photoreceptor cell death via receptor interacting protein 3 kinase mediated necroptosis
Por favor, use este identificador para citar o enlazar este ítem:
http://hdl.handle.net/10045/130406
Título: | UVA induces retinal photoreceptor cell death via receptor interacting protein 3 kinase mediated necroptosis |
---|---|
Autor/es: | Yu, Zhen | Correa, Victor S.M.C. | Efstathiou, Nikolaos E. | Albertos Arranz, Henar | Chen, Xiaohong | Ishihara, Kenji | Iesato, Yasuhiro | Narimatsu, Toshio | Ntentakis, Dimitrios | Vavvas, Demetrios G. |
Grupo/s de investigación o GITE: | Neurobiología del Sistema Visual y Terapia de Enfermedades Neurodegenerativas (NEUROVIS) |
Centro, Departamento o Servicio: | Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología |
Palabras clave: | UVA | Retinal photoreceptor | Cell death | Receptor interacting protein | 3 kinase | Necroptosis |
Fecha de publicación: | 12-dic-2022 |
Editor: | Springer Nature | CDD Press |
Cita bibliográfica: | Cell Death Discovery. 2022, 8:489. https://doi.org/10.1038/s41420-022-01273-1 |
Resumen: | Ultraviolet light A (UVA) is the only UV light that reaches the retina and can cause indirect damage to DNA via absorption of photons by non-DNA chromophores. Previous studies demonstrate that UVA generates reactive oxygen species (ROS) and leads to programmed cell death. Programmed cell death (PCD) has been implicated in numerous ophthalmologic diseases. Here, we investigated receptor interacting protein 1 and 3 (RIPK1 and RIPK3) kinases, key signaling molecules of PCD, in UVA-induced photoreceptor injury using in vitro and ex vivo models. UVA irradiation activated RIPK3 but not RIPK1 and mediated necroptosis through MLKL that lie downstream of RIPK3 and induced apoptosis through increased oxidative stress. Moreover, RIPK3 but not RIPK1 inhibition suppresses UVA-induced cell death along with the downregulation of MLKL and attenuates the levels of oxidative stress and DNA fragmentation. In conclusion, these results identify RIPK3, not RIPK1, as a critical regulator of UVA-induced necroptosis cell death in photoreceptors and highlight RIPK3 potential as a neuroprotective target. |
Patrocinador/es: | This work was supported by the Yeatts Family Foundation (D.G.V.); Monte J. Wallace (D.G.V.); 2013 Macula Society Research Grant Award (to D.G.V.); a Physician Scientist Award (to D.G.V.); unrestricted grant from the Research to Prevent Blindness Foundation (to J.W.M. and D.G.V.); National Eye Institute (NEI) R21EY023079-01/A1 (to D.G.V.); NEI Grant EY014104 (Massachusetts Eye and Ear Infirmary Core Grant) (to D.G.V.); Loeffler Family Fund (D.G.V.); R01EY025362-01 (to D.G.V.); ARI Young Investigator Award (to D.G.V.); Foundation Lions Eye Research Fund (D.G.V.); NIH NEI Core Grant P30EY003790 (to D.G.V.); Loeffler Family Fund (to D.G.V.); ARI Young Investigator Award (to D.G.V.). Shenzhen Science and Technology Program (Grant No. JCYJ20220530153607015); Shenzhen Science and Technology Program (Grant No. JCYJ20220531094004010); Shenzhen-Hong Kong Co-financing Project (Grant No. SGDX20190920110403741); Guangdong Basic and Applied Basic Research Foundation (No. 2022A1515012326); Shenzhen Science and Technology Program (Grant No. JSGG20201102174200001); Shenzhen Key Medical Discipline Construction Fund (No. SZXK038); Sanming Project of Medicine in Shenzhen (No. SZSM202011015); Shenzhen Fund for Guangdong Provincial High level Clinical Key Specialties (No. SZGSP014); National Natural Science Foundation of China (No. 82271103). |
URI: | http://hdl.handle.net/10045/130406 |
ISSN: | 10.1038/s41420-022-01273-1 | 2058-7716 |
Idioma: | eng |
Tipo: | info:eu-repo/semantics/article |
Derechos: | © The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
Revisión científica: | si |
Versión del editor: | https://doi.org/10.1038/s41420-022-01273-1 |
Aparece en las colecciones: | INV - NEUROVIS - Artículos de Revistas |
Archivos en este ítem:
Archivo | Descripción | Tamaño | Formato | |
---|---|---|---|---|
Yu_etal_2022_CellDeathDiscov.pdf | 5,06 MB | Adobe PDF | Abrir Vista previa | |
Este ítem está licenciado bajo Licencia Creative Commons