Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli

Autores
Goldstein Raij, Jorge; Carden, Tomas Roberto; Perez, María J.; Taira, Carlos Alberto; Höcht, Christian; Gironacci, Mariela Mercedes
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Shiga toxin 2 (Stx2)-producing enterohemorrhagic induced brain damage. Since a cerebroprotective action was reported for angiotensin (Ang)-(1–7), our aim was to investigate whether Ang-(1–7) protects from brain damage induced by Stx2-producing enterohemorrhagic Escherichia coli. The anterior hypothalamic area of adult male Wistar rats was injected with saline solution or Stx2 or Stx2 plus Ang-(1–7) or Stx2 plus Ang-(1–7) plus A779. Rats received a single injection of Stx2 at the beginning of the experiment, and Ang-(1–7), A779, or saline was administered daily in a single injection for 8 days. Cellular ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axonal demyelination, alterations in synapse, and oligodendrocyte and astrocyte damage, accompanied by edema. Ang-(1–7) prevented neuronal damage triggered by the toxin in 55.6 ± 9.5% of the neurons and the Stx2-induced synapse dysfunction was reversed. In addition, Ang-(1–7) blocked Stx2-induced demyelination in 92 ± 4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1–7) but astrocytes were only partially protected by the peptide (38 ± 5% of astrocytes were preserved). Ang-(1–7) treatment resulted in 50% reduction in the number of activated microglial cells induced by Stx2, suggesting an anti-inflammatory action. All these beneficial effects elicited by Ang-(1–7) were blocked by the Mas receptor antagonist and thus it was concluded that Ang-(1–7) protects mainly neurons and oligodendrocytes, and partially astrocytes, in the central nervous system through Mas receptor stimulation.
Fil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Carden, Tomas Roberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Perez, María J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Taira, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Gironacci, Mariela Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Materia
Angiotensin-(1-7)
Mas Receptor
Neuron
Oligodendrocyte
Astrocyte
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:11336/47423
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47423
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coliGoldstein Raij, JorgeCarden, Tomas RobertoPerez, María J.Taira, Carlos AlbertoHöcht, ChristianGironacci, Mariela MercedesAngiotensin-(1-7)Mas ReceptorNeuronOligodendrocyteAstrocytehttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Shiga toxin 2 (Stx2)-producing enterohemorrhagic induced brain damage. Since a cerebroprotective action was reported for angiotensin (Ang)-(1–7), our aim was to investigate whether Ang-(1–7) protects from brain damage induced by Stx2-producing enterohemorrhagic Escherichia coli. The anterior hypothalamic area of adult male Wistar rats was injected with saline solution or Stx2 or Stx2 plus Ang-(1–7) or Stx2 plus Ang-(1–7) plus A779. Rats received a single injection of Stx2 at the beginning of the experiment, and Ang-(1–7), A779, or saline was administered daily in a single injection for 8 days. Cellular ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axonal demyelination, alterations in synapse, and oligodendrocyte and astrocyte damage, accompanied by edema. Ang-(1–7) prevented neuronal damage triggered by the toxin in 55.6 ± 9.5% of the neurons and the Stx2-induced synapse dysfunction was reversed. In addition, Ang-(1–7) blocked Stx2-induced demyelination in 92 ± 4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1–7) but astrocytes were only partially protected by the peptide (38 ± 5% of astrocytes were preserved). Ang-(1–7) treatment resulted in 50% reduction in the number of activated microglial cells induced by Stx2, suggesting an anti-inflammatory action. All these beneficial effects elicited by Ang-(1–7) were blocked by the Mas receptor antagonist and thus it was concluded that Ang-(1–7) protects mainly neurons and oligodendrocytes, and partially astrocytes, in the central nervous system through Mas receptor stimulation.Fil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Carden, Tomas Roberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Perez, María J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Taira, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Gironacci, Mariela Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaAmerican Physiological Society2016-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/zipapplication/pdfhttp://hdl.handle.net/11336/47423Goldstein Raij, Jorge; Carden, Tomas Roberto; Perez, María J.; Taira, Carlos Alberto; Höcht, Christian; et al.; Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 311; 6; 12-2016; 1173-11850363-6119CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1152/ajpregu.00467.2015info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/10.1152/ajpregu.00467.2015info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:29Zoai:ri.conicet.gov.ar:11336/47423instacron: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:34982025-09-03 09:44:30.182CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
title Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
spellingShingle Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
Goldstein Raij, Jorge
Angiotensin-(1-7)
Mas Receptor
Neuron
Oligodendrocyte
Astrocyte
title_short Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
title_full Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
title_fullStr Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
title_full_unstemmed Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
title_sort Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli
dc.creator.none.fl_str_mv Goldstein Raij, Jorge
Carden, Tomas Roberto
Perez, María J.
Taira, Carlos Alberto
Höcht, Christian
Gironacci, Mariela Mercedes
author Goldstein Raij, Jorge
author_facet Goldstein Raij, Jorge
Carden, Tomas Roberto
Perez, María J.
Taira, Carlos Alberto
Höcht, Christian
Gironacci, Mariela Mercedes
author_role author
author2 Carden, Tomas Roberto
Perez, María J.
Taira, Carlos Alberto
Höcht, Christian
Gironacci, Mariela Mercedes
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Angiotensin-(1-7)
Mas Receptor
Neuron
Oligodendrocyte
Astrocyte
topic Angiotensin-(1-7)
Mas Receptor
Neuron
Oligodendrocyte
Astrocyte
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Shiga toxin 2 (Stx2)-producing enterohemorrhagic induced brain damage. Since a cerebroprotective action was reported for angiotensin (Ang)-(1–7), our aim was to investigate whether Ang-(1–7) protects from brain damage induced by Stx2-producing enterohemorrhagic Escherichia coli. The anterior hypothalamic area of adult male Wistar rats was injected with saline solution or Stx2 or Stx2 plus Ang-(1–7) or Stx2 plus Ang-(1–7) plus A779. Rats received a single injection of Stx2 at the beginning of the experiment, and Ang-(1–7), A779, or saline was administered daily in a single injection for 8 days. Cellular ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axonal demyelination, alterations in synapse, and oligodendrocyte and astrocyte damage, accompanied by edema. Ang-(1–7) prevented neuronal damage triggered by the toxin in 55.6 ± 9.5% of the neurons and the Stx2-induced synapse dysfunction was reversed. In addition, Ang-(1–7) blocked Stx2-induced demyelination in 92 ± 4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1–7) but astrocytes were only partially protected by the peptide (38 ± 5% of astrocytes were preserved). Ang-(1–7) treatment resulted in 50% reduction in the number of activated microglial cells induced by Stx2, suggesting an anti-inflammatory action. All these beneficial effects elicited by Ang-(1–7) were blocked by the Mas receptor antagonist and thus it was concluded that Ang-(1–7) protects mainly neurons and oligodendrocytes, and partially astrocytes, in the central nervous system through Mas receptor stimulation.
Fil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Carden, Tomas Roberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Perez, María J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Taira, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Gironacci, Mariela Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
description Shiga toxin 2 (Stx2)-producing enterohemorrhagic induced brain damage. Since a cerebroprotective action was reported for angiotensin (Ang)-(1–7), our aim was to investigate whether Ang-(1–7) protects from brain damage induced by Stx2-producing enterohemorrhagic Escherichia coli. The anterior hypothalamic area of adult male Wistar rats was injected with saline solution or Stx2 or Stx2 plus Ang-(1–7) or Stx2 plus Ang-(1–7) plus A779. Rats received a single injection of Stx2 at the beginning of the experiment, and Ang-(1–7), A779, or saline was administered daily in a single injection for 8 days. Cellular ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axonal demyelination, alterations in synapse, and oligodendrocyte and astrocyte damage, accompanied by edema. Ang-(1–7) prevented neuronal damage triggered by the toxin in 55.6 ± 9.5% of the neurons and the Stx2-induced synapse dysfunction was reversed. In addition, Ang-(1–7) blocked Stx2-induced demyelination in 92 ± 4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1–7) but astrocytes were only partially protected by the peptide (38 ± 5% of astrocytes were preserved). Ang-(1–7) treatment resulted in 50% reduction in the number of activated microglial cells induced by Stx2, suggesting an anti-inflammatory action. All these beneficial effects elicited by Ang-(1–7) were blocked by the Mas receptor antagonist and thus it was concluded that Ang-(1–7) protects mainly neurons and oligodendrocytes, and partially astrocytes, in the central nervous system through Mas receptor stimulation.
publishDate 2016
dc.date.none.fl_str_mv 2016-12
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/11336/47423
Goldstein Raij, Jorge; Carden, Tomas Roberto; Perez, María J.; Taira, Carlos Alberto; Höcht, Christian; et al.; Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 311; 6; 12-2016; 1173-1185
0363-6119
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47423
identifier_str_mv Goldstein Raij, Jorge; Carden, Tomas Roberto; Perez, María J.; Taira, Carlos Alberto; Höcht, Christian; et al.; Angiotensin-(1–7) protects from brain damage induced by shiga toxin 2-producing enterohemorrhagic Escherichia coli; American Physiological Society; American Journal Of Physiology-regulatory, Integrative And Comparative Physiology; 311; 6; 12-2016; 1173-1185
0363-6119
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpregu.00467.2015
info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/10.1152/ajpregu.00467.2015
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/zip
application/pdf
dc.publisher.none.fl_str_mv American Physiological Society
publisher.none.fl_str_mv American Physiological Society
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 13.13397

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