Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus

Autores
Troncoso, Mariana Elizabeth; Bannoud, Nadia; Carvelli, Flavia Lorena; Asensio, Joana Antonela; Seltzer, Alicia Mabel; Sosa Escudero, Miguel Angel
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Neuronal excitotoxicity induced by glutamatergic receptor overstimulation contributes to brain damage. Recent studies have shown that lysosomal membrane permeabilization (LMP) is involved in ischemia-associated neuronal death. In this study we evaluated the effect of neonatal hypoxia-ischemia (HI), as a model of excitotoxicity, on the lysosomal integrity throughout the distribution of the lysosomal proteins cathepsin D and prosaposin. Rat pups (7 days old) of the Wistar Kyoto strain were submitted to HI and they were euthanized 4 days after treatment and the cerebral cortex (Cx) and hippocampus (HIP) were processed for immunohistochemistry or immunoblotting. Treatment induced an increase of gliosis and also a redistribution of both prosaposin and cathepsin D (as intermediate and mature forms), into the cytosol of the HIP and Cx. In addition, HI induced a decrease of LAMP-1 in the membranous fraction and the appearance of a reactive band to anti-LAMP-1 in the cytosolic fraction, suggesting a cleavage of this protein. From these results, we propose that the abnormal release of Cat D and PSAP to the cytosol is triggered as a result of LAMP-1 cleavage in HI animals, which leads to cell damage. This could be a common mechanism in pathological conditions that compromises neuronal survival and brain function.
Fil: Troncoso, Mariana Elizabeth. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Bannoud, Nadia. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Carvelli, Flavia Lorena. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Asensio, Joana Antonela. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Seltzer, Alicia Mabel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Sosa Escudero, Miguel Angel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina. Universidad Nacional de Cuyo; Argentina
Materia
EXCITOTOXICITY
HYPOXIA-ISCHEMIA
LYSOSOMAL ENZYMES
LYSOSOMES
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:11336/92605
Acceder
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network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampusTroncoso, Mariana ElizabethBannoud, NadiaCarvelli, Flavia LorenaAsensio, Joana AntonelaSeltzer, Alicia MabelSosa Escudero, Miguel AngelEXCITOTOXICITYHYPOXIA-ISCHEMIALYSOSOMAL ENZYMESLYSOSOMEShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Neuronal excitotoxicity induced by glutamatergic receptor overstimulation contributes to brain damage. Recent studies have shown that lysosomal membrane permeabilization (LMP) is involved in ischemia-associated neuronal death. In this study we evaluated the effect of neonatal hypoxia-ischemia (HI), as a model of excitotoxicity, on the lysosomal integrity throughout the distribution of the lysosomal proteins cathepsin D and prosaposin. Rat pups (7 days old) of the Wistar Kyoto strain were submitted to HI and they were euthanized 4 days after treatment and the cerebral cortex (Cx) and hippocampus (HIP) were processed for immunohistochemistry or immunoblotting. Treatment induced an increase of gliosis and also a redistribution of both prosaposin and cathepsin D (as intermediate and mature forms), into the cytosol of the HIP and Cx. In addition, HI induced a decrease of LAMP-1 in the membranous fraction and the appearance of a reactive band to anti-LAMP-1 in the cytosolic fraction, suggesting a cleavage of this protein. From these results, we propose that the abnormal release of Cat D and PSAP to the cytosol is triggered as a result of LAMP-1 cleavage in HI animals, which leads to cell damage. This could be a common mechanism in pathological conditions that compromises neuronal survival and brain function.Fil: Troncoso, Mariana Elizabeth. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; ArgentinaFil: Bannoud, Nadia. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; ArgentinaFil: Carvelli, Flavia Lorena. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; ArgentinaFil: Asensio, Joana Antonela. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; ArgentinaFil: Seltzer, Alicia Mabel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; ArgentinaFil: Sosa Escudero, Miguel Angel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina. Universidad Nacional de Cuyo; ArgentinaCompany of Biologists2018-10-25info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/92605Troncoso, Mariana Elizabeth; Bannoud, Nadia; Carvelli, Flavia Lorena; Asensio, Joana Antonela; Seltzer, Alicia Mabel; et al.; Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus; Company of Biologists; Biology Open; 7; 10; 25-10-2018; 1-82046-6390CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://bio.biologists.org/lookup/doi/10.1242/bio.036723info:eu-repo/semantics/altIdentifier/doi/10.1242/bio.036723info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:45:58Zoai:ri.conicet.gov.ar:11336/92605instacron: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 09:45:59.122CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
title Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
spellingShingle Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
Troncoso, Mariana Elizabeth
EXCITOTOXICITY
HYPOXIA-ISCHEMIA
LYSOSOMAL ENZYMES
LYSOSOMES
title_short Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
title_full Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
title_fullStr Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
title_full_unstemmed Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
title_sort Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus
dc.creator.none.fl_str_mv Troncoso, Mariana Elizabeth
Bannoud, Nadia
Carvelli, Flavia Lorena
Asensio, Joana Antonela
Seltzer, Alicia Mabel
Sosa Escudero, Miguel Angel
author Troncoso, Mariana Elizabeth
author_facet Troncoso, Mariana Elizabeth
Bannoud, Nadia
Carvelli, Flavia Lorena
Asensio, Joana Antonela
Seltzer, Alicia Mabel
Sosa Escudero, Miguel Angel
author_role author
author2 Bannoud, Nadia
Carvelli, Flavia Lorena
Asensio, Joana Antonela
Seltzer, Alicia Mabel
Sosa Escudero, Miguel Angel
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv EXCITOTOXICITY
HYPOXIA-ISCHEMIA
LYSOSOMAL ENZYMES
LYSOSOMES
topic EXCITOTOXICITY
HYPOXIA-ISCHEMIA
LYSOSOMAL ENZYMES
LYSOSOMES
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Neuronal excitotoxicity induced by glutamatergic receptor overstimulation contributes to brain damage. Recent studies have shown that lysosomal membrane permeabilization (LMP) is involved in ischemia-associated neuronal death. In this study we evaluated the effect of neonatal hypoxia-ischemia (HI), as a model of excitotoxicity, on the lysosomal integrity throughout the distribution of the lysosomal proteins cathepsin D and prosaposin. Rat pups (7 days old) of the Wistar Kyoto strain were submitted to HI and they were euthanized 4 days after treatment and the cerebral cortex (Cx) and hippocampus (HIP) were processed for immunohistochemistry or immunoblotting. Treatment induced an increase of gliosis and also a redistribution of both prosaposin and cathepsin D (as intermediate and mature forms), into the cytosol of the HIP and Cx. In addition, HI induced a decrease of LAMP-1 in the membranous fraction and the appearance of a reactive band to anti-LAMP-1 in the cytosolic fraction, suggesting a cleavage of this protein. From these results, we propose that the abnormal release of Cat D and PSAP to the cytosol is triggered as a result of LAMP-1 cleavage in HI animals, which leads to cell damage. This could be a common mechanism in pathological conditions that compromises neuronal survival and brain function.
Fil: Troncoso, Mariana Elizabeth. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Bannoud, Nadia. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Carvelli, Flavia Lorena. Universidad Nacional de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Asensio, Joana Antonela. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Seltzer, Alicia Mabel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina
Fil: Sosa Escudero, Miguel Angel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología; Argentina. Universidad Nacional de Cuyo; Argentina
description Neuronal excitotoxicity induced by glutamatergic receptor overstimulation contributes to brain damage. Recent studies have shown that lysosomal membrane permeabilization (LMP) is involved in ischemia-associated neuronal death. In this study we evaluated the effect of neonatal hypoxia-ischemia (HI), as a model of excitotoxicity, on the lysosomal integrity throughout the distribution of the lysosomal proteins cathepsin D and prosaposin. Rat pups (7 days old) of the Wistar Kyoto strain were submitted to HI and they were euthanized 4 days after treatment and the cerebral cortex (Cx) and hippocampus (HIP) were processed for immunohistochemistry or immunoblotting. Treatment induced an increase of gliosis and also a redistribution of both prosaposin and cathepsin D (as intermediate and mature forms), into the cytosol of the HIP and Cx. In addition, HI induced a decrease of LAMP-1 in the membranous fraction and the appearance of a reactive band to anti-LAMP-1 in the cytosolic fraction, suggesting a cleavage of this protein. From these results, we propose that the abnormal release of Cat D and PSAP to the cytosol is triggered as a result of LAMP-1 cleavage in HI animals, which leads to cell damage. This could be a common mechanism in pathological conditions that compromises neuronal survival and brain function.
publishDate 2018
dc.date.none.fl_str_mv 2018-10-25
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/92605
Troncoso, Mariana Elizabeth; Bannoud, Nadia; Carvelli, Flavia Lorena; Asensio, Joana Antonela; Seltzer, Alicia Mabel; et al.; Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus; Company of Biologists; Biology Open; 7; 10; 25-10-2018; 1-8
2046-6390
CONICET Digital
CONICET
url http://hdl.handle.net/11336/92605
identifier_str_mv Troncoso, Mariana Elizabeth; Bannoud, Nadia; Carvelli, Flavia Lorena; Asensio, Joana Antonela; Seltzer, Alicia Mabel; et al.; Hypoxia-ischemia alters distribution of lysosomal proteins in rat cortex and hippocampus; Company of Biologists; Biology Open; 7; 10; 25-10-2018; 1-8
2046-6390
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://bio.biologists.org/lookup/doi/10.1242/bio.036723
info:eu-repo/semantics/altIdentifier/doi/10.1242/bio.036723
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
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Company of Biologists
publisher.none.fl_str_mv Company of Biologists
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.069144

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