Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?

Autores
Aguilera, Aída J.; Otero-losada, Matilde Estela; Cao, Gabriel Fernando; Serafini, Enriqueta M.; Muller, Angelica del Carmen; Azzato, Francisco; Milei, Jose
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Aim. To evaluate the sequence of biochemical and pathological changes in liver and abdominal aorta in apolipoprotein-E deficient mice (8 weeks old, standard diet) in relation with age. Materials and methods: euthanasia (pentobarbital sodium and phenytoin) was practiced at 16, 20 and 30 weeks of age. Glycemia and the level of total cholesterol and its fractions were biochemically routinely determined. Sections of the liver and the ascending aorta were dissected and conventionally processed for morphology and morphometry. Results: hyperglycemia was observed at 20 weeks (39%, p<0.02). Hypertriglyceridemia (x2.8, p<0.01), an increase in non-HDL cholesterol (71%, p<0.05) and a decrease in HDL cholesterol (-26%, p<0.05) were found at 30 weeks. Liver inflammation and portal inflammation increased (4-fold, p<0.01 and 2-fold, p<0.03 respectively) between weeks 20-30. At week 30: aortic plaque area and the percentage of stenosis increased (respectively 5-fold, p<0.0001 and 2.4-fold, p<0.01) and the intima-media ratio increased (3-fold, p<0.05) with media thinning (-69 %, p<0.01). Preatherosclerotic lesions consisted of subendothelial clusters of foamy cells in contrast with intimal thickening due to smooth muscle cell proliferation as typically found in man. Conclusion: ApoE-/- mice spontaneously developed early hyperglycemia, followed by dyslipidemia with hypertriglyceridemia, and hepatic and aortic pathology. The sequence of the changes suggests that hypertriglyceridemia, decreased levels of HDL and hepatic inflammation favored aortic damage progression. Otherwise morphologically similar, the sequence of events resulting in plaque formation is different to that found in man. Bearing this in mind, the ApoE-/- mice model may be used to study the biochemical and molecular events underlying atherosclerosis.
Fil: Aguilera, Aída J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Otero-losada, Matilde Estela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Serafini, Enriqueta M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Muller, Angelica del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Azzato, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Milei, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Materia
Apo e Mice
Biochemical
Atherosclerosis
Aorta
Liver
Hypertriglyceridemia
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:11336/7902
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/7902
network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?Biochemical Changes and Aortic Atherosclerosis in a Colony of Apolipoprotein-E Deficient Mice: A Possible Model?Aguilera, Aída J.Otero-losada, Matilde EstelaCao, Gabriel FernandoSerafini, Enriqueta M.Muller, Angelica del CarmenAzzato, FranciscoMilei, JoseApo e MiceBiochemicalAtherosclerosisAortaLiverHypertriglyceridemiahttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Aim. To evaluate the sequence of biochemical and pathological changes in liver and abdominal aorta in apolipoprotein-E deficient mice (8 weeks old, standard diet) in relation with age. Materials and methods: euthanasia (pentobarbital sodium and phenytoin) was practiced at 16, 20 and 30 weeks of age. Glycemia and the level of total cholesterol and its fractions were biochemically routinely determined. Sections of the liver and the ascending aorta were dissected and conventionally processed for morphology and morphometry. Results: hyperglycemia was observed at 20 weeks (39%, p<0.02). Hypertriglyceridemia (x2.8, p<0.01), an increase in non-HDL cholesterol (71%, p<0.05) and a decrease in HDL cholesterol (-26%, p<0.05) were found at 30 weeks. Liver inflammation and portal inflammation increased (4-fold, p<0.01 and 2-fold, p<0.03 respectively) between weeks 20-30. At week 30: aortic plaque area and the percentage of stenosis increased (respectively 5-fold, p<0.0001 and 2.4-fold, p<0.01) and the intima-media ratio increased (3-fold, p<0.05) with media thinning (-69 %, p<0.01). Preatherosclerotic lesions consisted of subendothelial clusters of foamy cells in contrast with intimal thickening due to smooth muscle cell proliferation as typically found in man. Conclusion: ApoE-/- mice spontaneously developed early hyperglycemia, followed by dyslipidemia with hypertriglyceridemia, and hepatic and aortic pathology. The sequence of the changes suggests that hypertriglyceridemia, decreased levels of HDL and hepatic inflammation favored aortic damage progression. Otherwise morphologically similar, the sequence of events resulting in plaque formation is different to that found in man. Bearing this in mind, the ApoE-/- mice model may be used to study the biochemical and molecular events underlying atherosclerosis.Fil: Aguilera, Aída J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Otero-losada, Matilde Estela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Serafini, Enriqueta M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Muller, Angelica del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Azzato, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaFil: Milei, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); ArgentinaSociedad Argentina de Cardiología2014-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/7902Aguilera, Aída J.; Otero-losada, Matilde Estela; Cao, Gabriel Fernando; Serafini, Enriqueta M.; Muller, Angelica del Carmen; et al.; Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?; Sociedad Argentina de Cardiología; Revista de la Federación Argentina de Cardiología; 43; 4; 12-2014; 176-1811666-5694enginfo:eu-repo/semantics/altIdentifier/url/https://www.fac.org.ar/archivo/2/revista/14v43n4/art_orig/art_orig01/aguilera_ingles.phpinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:06:11Zoai:ri.conicet.gov.ar:11336/7902instacron: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 10:06:12.096CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
Biochemical Changes and Aortic Atherosclerosis in a Colony of Apolipoprotein-E Deficient Mice: A Possible Model?
title Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
spellingShingle Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
Aguilera, Aída J.
Apo e Mice
Biochemical
Atherosclerosis
Aorta
Liver
Hypertriglyceridemia
title_short Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
title_full Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
title_fullStr Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
title_full_unstemmed Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
title_sort Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?
dc.creator.none.fl_str_mv Aguilera, Aída J.
Otero-losada, Matilde Estela
Cao, Gabriel Fernando
Serafini, Enriqueta M.
Muller, Angelica del Carmen
Azzato, Francisco
Milei, Jose
author Aguilera, Aída J.
author_facet Aguilera, Aída J.
Otero-losada, Matilde Estela
Cao, Gabriel Fernando
Serafini, Enriqueta M.
Muller, Angelica del Carmen
Azzato, Francisco
Milei, Jose
author_role author
author2 Otero-losada, Matilde Estela
Cao, Gabriel Fernando
Serafini, Enriqueta M.
Muller, Angelica del Carmen
Azzato, Francisco
Milei, Jose
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Apo e Mice
Biochemical
Atherosclerosis
Aorta
Liver
Hypertriglyceridemia
topic Apo e Mice
Biochemical
Atherosclerosis
Aorta
Liver
Hypertriglyceridemia
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Aim. To evaluate the sequence of biochemical and pathological changes in liver and abdominal aorta in apolipoprotein-E deficient mice (8 weeks old, standard diet) in relation with age. Materials and methods: euthanasia (pentobarbital sodium and phenytoin) was practiced at 16, 20 and 30 weeks of age. Glycemia and the level of total cholesterol and its fractions were biochemically routinely determined. Sections of the liver and the ascending aorta were dissected and conventionally processed for morphology and morphometry. Results: hyperglycemia was observed at 20 weeks (39%, p<0.02). Hypertriglyceridemia (x2.8, p<0.01), an increase in non-HDL cholesterol (71%, p<0.05) and a decrease in HDL cholesterol (-26%, p<0.05) were found at 30 weeks. Liver inflammation and portal inflammation increased (4-fold, p<0.01 and 2-fold, p<0.03 respectively) between weeks 20-30. At week 30: aortic plaque area and the percentage of stenosis increased (respectively 5-fold, p<0.0001 and 2.4-fold, p<0.01) and the intima-media ratio increased (3-fold, p<0.05) with media thinning (-69 %, p<0.01). Preatherosclerotic lesions consisted of subendothelial clusters of foamy cells in contrast with intimal thickening due to smooth muscle cell proliferation as typically found in man. Conclusion: ApoE-/- mice spontaneously developed early hyperglycemia, followed by dyslipidemia with hypertriglyceridemia, and hepatic and aortic pathology. The sequence of the changes suggests that hypertriglyceridemia, decreased levels of HDL and hepatic inflammation favored aortic damage progression. Otherwise morphologically similar, the sequence of events resulting in plaque formation is different to that found in man. Bearing this in mind, the ApoE-/- mice model may be used to study the biochemical and molecular events underlying atherosclerosis.
Fil: Aguilera, Aída J.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Otero-losada, Matilde Estela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Cao, Gabriel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Serafini, Enriqueta M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Muller, Angelica del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Azzato, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
Fil: Milei, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas (i); Argentina
description Aim. To evaluate the sequence of biochemical and pathological changes in liver and abdominal aorta in apolipoprotein-E deficient mice (8 weeks old, standard diet) in relation with age. Materials and methods: euthanasia (pentobarbital sodium and phenytoin) was practiced at 16, 20 and 30 weeks of age. Glycemia and the level of total cholesterol and its fractions were biochemically routinely determined. Sections of the liver and the ascending aorta were dissected and conventionally processed for morphology and morphometry. Results: hyperglycemia was observed at 20 weeks (39%, p<0.02). Hypertriglyceridemia (x2.8, p<0.01), an increase in non-HDL cholesterol (71%, p<0.05) and a decrease in HDL cholesterol (-26%, p<0.05) were found at 30 weeks. Liver inflammation and portal inflammation increased (4-fold, p<0.01 and 2-fold, p<0.03 respectively) between weeks 20-30. At week 30: aortic plaque area and the percentage of stenosis increased (respectively 5-fold, p<0.0001 and 2.4-fold, p<0.01) and the intima-media ratio increased (3-fold, p<0.05) with media thinning (-69 %, p<0.01). Preatherosclerotic lesions consisted of subendothelial clusters of foamy cells in contrast with intimal thickening due to smooth muscle cell proliferation as typically found in man. Conclusion: ApoE-/- mice spontaneously developed early hyperglycemia, followed by dyslipidemia with hypertriglyceridemia, and hepatic and aortic pathology. The sequence of the changes suggests that hypertriglyceridemia, decreased levels of HDL and hepatic inflammation favored aortic damage progression. Otherwise morphologically similar, the sequence of events resulting in plaque formation is different to that found in man. Bearing this in mind, the ApoE-/- mice model may be used to study the biochemical and molecular events underlying atherosclerosis.
publishDate 2014
dc.date.none.fl_str_mv 2014-12
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/11336/7902
Aguilera, Aída J.; Otero-losada, Matilde Estela; Cao, Gabriel Fernando; Serafini, Enriqueta M.; Muller, Angelica del Carmen; et al.; Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?; Sociedad Argentina de Cardiología; Revista de la Federación Argentina de Cardiología; 43; 4; 12-2014; 176-181
1666-5694
url http://hdl.handle.net/11336/7902
identifier_str_mv Aguilera, Aída J.; Otero-losada, Matilde Estela; Cao, Gabriel Fernando; Serafini, Enriqueta M.; Muller, Angelica del Carmen; et al.; Hallazgos bioquímicos y ateroescleróticos en una colonia de ratones deficientes en apolipoproteina E: ¿Un modelo posible?; Sociedad Argentina de Cardiología; Revista de la Federación Argentina de Cardiología; 43; 4; 12-2014; 176-181
1666-5694
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.fac.org.ar/archivo/2/revista/14v43n4/art_orig/art_orig01/aguilera_ingles.php
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
dc.publisher.none.fl_str_mv Sociedad Argentina de Cardiología
publisher.none.fl_str_mv Sociedad Argentina de Cardiología
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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