Light, lipids and photoreceptor survival: live or let die?

Autores
Rotstein, Nora Patricia; German, Olga Lorena; Agnolazza, Daniela Luciana; Politi, Luis Enrique
Año de publicación
2014
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Due to its constant exposure to light and its high oxygen consumption the retina is highly sensitive to oxidative damage, which is involved in the death of photoreceptors in retinal neurodegenerative diseases such as retinitis pigmentosa and age related macular degeneration. A peculiar characteristic of retina lipids, their high content of polyunsaturated fatty acids, mainly docosahexaenoico acid (DHA), has also been proposed to contribute to this sensitivity. However, the role of DHA in the retina is still controversial. Its six double bonds make it highly prone to peroxidation and it has been shown to increase retina vulnerability to photo-oxidative damage. However, DHA has also a protective role on photoreceptors. Our lab has shown that DHA protects photoreceptors from oxidative stress by activating the ERK/MAPK pathway. We now investigated how DHA activated this pathway and if it also activated antioxidant defense mechanisms in photoreceptors. Addition of retinoid X receptors (RXR) antagonists to rat retinal neuronal cultures inhibited DHA protection during early development in vitro and upon oxidative stress. Inhibition of an alternative pathway, involving tyrosine kinase (Trk) receptors, did not affect DHA prevention of photoreceptor apoptosis. These results imply that activation of RXR was required for DHA protection. H2O2 treatment increased reactive oxygen species (ROS) production in retinal neurons, inducing photoreceptor apoptosis. DHA prevented H2O2-induced apoptosis, simultaneously decreasing ROS formation. Analysis of enzymatic activity evidenced that DHA addition increased glutathione peroxidase activity in cultures treated with or without H2O2. Our results provide the first evidence that DHA activates RXR to prevent photoreceptor death. They also suggest that DHA activation of antioxidant defense mechanisms is at least in part responsible of protecting photoreceptors from oxidative stress
Fil: Rotstein, Nora Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: German, Olga Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Agnolazza, Daniela Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Politi, Luis Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
16th International Congress on Photobiology
Córdoba
Argentina
International Union of Photobiology
Materia
PHOTORECEPTOR
RETINA
DOCOSAHEXAENOIC ACID
RETINOID X RECEPTOR
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/235877

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network_name_str CONICET Digital (CONICET)
spelling Light, lipids and photoreceptor survival: live or let die?Rotstein, Nora PatriciaGerman, Olga LorenaAgnolazza, Daniela LucianaPoliti, Luis EnriquePHOTORECEPTORRETINADOCOSAHEXAENOIC ACIDRETINOID X RECEPTORhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Due to its constant exposure to light and its high oxygen consumption the retina is highly sensitive to oxidative damage, which is involved in the death of photoreceptors in retinal neurodegenerative diseases such as retinitis pigmentosa and age related macular degeneration. A peculiar characteristic of retina lipids, their high content of polyunsaturated fatty acids, mainly docosahexaenoico acid (DHA), has also been proposed to contribute to this sensitivity. However, the role of DHA in the retina is still controversial. Its six double bonds make it highly prone to peroxidation and it has been shown to increase retina vulnerability to photo-oxidative damage. However, DHA has also a protective role on photoreceptors. Our lab has shown that DHA protects photoreceptors from oxidative stress by activating the ERK/MAPK pathway. We now investigated how DHA activated this pathway and if it also activated antioxidant defense mechanisms in photoreceptors. Addition of retinoid X receptors (RXR) antagonists to rat retinal neuronal cultures inhibited DHA protection during early development in vitro and upon oxidative stress. Inhibition of an alternative pathway, involving tyrosine kinase (Trk) receptors, did not affect DHA prevention of photoreceptor apoptosis. These results imply that activation of RXR was required for DHA protection. H2O2 treatment increased reactive oxygen species (ROS) production in retinal neurons, inducing photoreceptor apoptosis. DHA prevented H2O2-induced apoptosis, simultaneously decreasing ROS formation. Analysis of enzymatic activity evidenced that DHA addition increased glutathione peroxidase activity in cultures treated with or without H2O2. Our results provide the first evidence that DHA activates RXR to prevent photoreceptor death. They also suggest that DHA activation of antioxidant defense mechanisms is at least in part responsible of protecting photoreceptors from oxidative stressFil: Rotstein, Nora Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: German, Olga Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Agnolazza, Daniela Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Politi, Luis Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina16th International Congress on PhotobiologyCórdobaArgentinaInternational Union of PhotobiologyInternational Union of Photobiology2014info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/235877Light, lipids and photoreceptor survival: live or let die?; 16th International Congress on Photobiology; Córdoba; Argentina; 2014; 252-252CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://grupoargentinodefotobiologia.info/site/site/grupar/pluginfile.php/86/block_html/content/16icp-libro.pdfInternacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:40:45Zoai:ri.conicet.gov.ar:11336/235877instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:40:45.336CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Light, lipids and photoreceptor survival: live or let die?
title Light, lipids and photoreceptor survival: live or let die?
spellingShingle Light, lipids and photoreceptor survival: live or let die?
Rotstein, Nora Patricia
PHOTORECEPTOR
RETINA
DOCOSAHEXAENOIC ACID
RETINOID X RECEPTOR
title_short Light, lipids and photoreceptor survival: live or let die?
title_full Light, lipids and photoreceptor survival: live or let die?
title_fullStr Light, lipids and photoreceptor survival: live or let die?
title_full_unstemmed Light, lipids and photoreceptor survival: live or let die?
title_sort Light, lipids and photoreceptor survival: live or let die?
dc.creator.none.fl_str_mv Rotstein, Nora Patricia
German, Olga Lorena
Agnolazza, Daniela Luciana
Politi, Luis Enrique
author Rotstein, Nora Patricia
author_facet Rotstein, Nora Patricia
German, Olga Lorena
Agnolazza, Daniela Luciana
Politi, Luis Enrique
author_role author
author2 German, Olga Lorena
Agnolazza, Daniela Luciana
Politi, Luis Enrique
author2_role author
author
author
dc.subject.none.fl_str_mv PHOTORECEPTOR
RETINA
DOCOSAHEXAENOIC ACID
RETINOID X RECEPTOR
topic PHOTORECEPTOR
RETINA
DOCOSAHEXAENOIC ACID
RETINOID X RECEPTOR
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Due to its constant exposure to light and its high oxygen consumption the retina is highly sensitive to oxidative damage, which is involved in the death of photoreceptors in retinal neurodegenerative diseases such as retinitis pigmentosa and age related macular degeneration. A peculiar characteristic of retina lipids, their high content of polyunsaturated fatty acids, mainly docosahexaenoico acid (DHA), has also been proposed to contribute to this sensitivity. However, the role of DHA in the retina is still controversial. Its six double bonds make it highly prone to peroxidation and it has been shown to increase retina vulnerability to photo-oxidative damage. However, DHA has also a protective role on photoreceptors. Our lab has shown that DHA protects photoreceptors from oxidative stress by activating the ERK/MAPK pathway. We now investigated how DHA activated this pathway and if it also activated antioxidant defense mechanisms in photoreceptors. Addition of retinoid X receptors (RXR) antagonists to rat retinal neuronal cultures inhibited DHA protection during early development in vitro and upon oxidative stress. Inhibition of an alternative pathway, involving tyrosine kinase (Trk) receptors, did not affect DHA prevention of photoreceptor apoptosis. These results imply that activation of RXR was required for DHA protection. H2O2 treatment increased reactive oxygen species (ROS) production in retinal neurons, inducing photoreceptor apoptosis. DHA prevented H2O2-induced apoptosis, simultaneously decreasing ROS formation. Analysis of enzymatic activity evidenced that DHA addition increased glutathione peroxidase activity in cultures treated with or without H2O2. Our results provide the first evidence that DHA activates RXR to prevent photoreceptor death. They also suggest that DHA activation of antioxidant defense mechanisms is at least in part responsible of protecting photoreceptors from oxidative stress
Fil: Rotstein, Nora Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: German, Olga Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Agnolazza, Daniela Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Politi, Luis Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
16th International Congress on Photobiology
Córdoba
Argentina
International Union of Photobiology
description Due to its constant exposure to light and its high oxygen consumption the retina is highly sensitive to oxidative damage, which is involved in the death of photoreceptors in retinal neurodegenerative diseases such as retinitis pigmentosa and age related macular degeneration. A peculiar characteristic of retina lipids, their high content of polyunsaturated fatty acids, mainly docosahexaenoico acid (DHA), has also been proposed to contribute to this sensitivity. However, the role of DHA in the retina is still controversial. Its six double bonds make it highly prone to peroxidation and it has been shown to increase retina vulnerability to photo-oxidative damage. However, DHA has also a protective role on photoreceptors. Our lab has shown that DHA protects photoreceptors from oxidative stress by activating the ERK/MAPK pathway. We now investigated how DHA activated this pathway and if it also activated antioxidant defense mechanisms in photoreceptors. Addition of retinoid X receptors (RXR) antagonists to rat retinal neuronal cultures inhibited DHA protection during early development in vitro and upon oxidative stress. Inhibition of an alternative pathway, involving tyrosine kinase (Trk) receptors, did not affect DHA prevention of photoreceptor apoptosis. These results imply that activation of RXR was required for DHA protection. H2O2 treatment increased reactive oxygen species (ROS) production in retinal neurons, inducing photoreceptor apoptosis. DHA prevented H2O2-induced apoptosis, simultaneously decreasing ROS formation. Analysis of enzymatic activity evidenced that DHA addition increased glutathione peroxidase activity in cultures treated with or without H2O2. Our results provide the first evidence that DHA activates RXR to prevent photoreceptor death. They also suggest that DHA activation of antioxidant defense mechanisms is at least in part responsible of protecting photoreceptors from oxidative stress
publishDate 2014
dc.date.none.fl_str_mv 2014
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Congreso
Book
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/235877
Light, lipids and photoreceptor survival: live or let die?; 16th International Congress on Photobiology; Córdoba; Argentina; 2014; 252-252
CONICET Digital
CONICET
url http://hdl.handle.net/11336/235877
identifier_str_mv Light, lipids and photoreceptor survival: live or let die?; 16th International Congress on Photobiology; Córdoba; Argentina; 2014; 252-252
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://grupoargentinodefotobiologia.info/site/site/grupar/pluginfile.php/86/block_html/content/16icp-libro.pdf
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv International Union of Photobiology
publisher.none.fl_str_mv International Union of Photobiology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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