Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding

Autores
Todaro, Juan Santiago; Stoyanoff, Tania Romina; Aguirre, María Victoria; Brandan, Nora Cristina
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The underlying interactions among apoptosis, erythroid proliferation and differentiation involved in bone marrow erythropoietic response after an acute blood-loss have not yet been elucidated in detail. We hypothesized that Erythropoietin receptor, Bax, caspase-3, cytochrome c, Smac/DIABLO and Bcl-xL molecules play important roles at time of acute erythropoietic need to ameliorate the hypoxic stress. Experiments were performed using in vivo murine model of anaemia induced by blood-loss in a time course study of 15 days. Haematological parameters and bone marrow cellularities were determined. Bone marrow apoptotic assays included: double fluorescent staining (acridine orange/ethidium bromide) and TUNEL. Bone marrow clonogenic assays were performed for evaluating erythroid colony forming unit?s expansion. The Erythropoietin receptor, Bax, Bcl-xL, Smac/DIABLO, caspase-3 and cytochrome c expressions were assessed by immunoblottings. Caspase-3 activity was determined with a colorimetric assay kit. Bleeding induces bone marrow apoptosis from 1 to 3 days, concomitant with Bax over-expression and Bcl-xL decrease. The mitochondrial dysfunction caused cytochrome c and Smac/DIABLO release to cytosol and caspase-3 activation. Erythropoietic recovery was associated with Erythropoietin receptor over expression from the third day, concomitant with the erythroid progenitors and Bcl-xL/Bax ratio enhancements. Erythropoiesis after bleeding depends on a delicate balance among proapoptotic (Bax, caspase-3, cytochrome c, Smac/DIABLO) and prosurvival proteins (Erythropoietin receptor, Bcl-xL), as the crucial regulators in bone marrow erythroid recovery. These findings provide new insights into the homeostatic mechanisms which promote erythropoietic response post-bleeding.
Fil: Todaro, Juan Santiago. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Stoyanoff, Tania Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; Argentina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Aguirre, María Victoria. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Brandan, Nora Cristina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; Argentina
Materia
Apoptosis
Bleeding
Bone Marrow
Caspase 3
Erythropoietin 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:11336/77459
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/77459
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by BleedingTodaro, Juan SantiagoStoyanoff, Tania RominaAguirre, María VictoriaBrandan, Nora CristinaApoptosisBleedingBone MarrowCaspase 3Erythropoietin Receptorhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The underlying interactions among apoptosis, erythroid proliferation and differentiation involved in bone marrow erythropoietic response after an acute blood-loss have not yet been elucidated in detail. We hypothesized that Erythropoietin receptor, Bax, caspase-3, cytochrome c, Smac/DIABLO and Bcl-xL molecules play important roles at time of acute erythropoietic need to ameliorate the hypoxic stress. Experiments were performed using in vivo murine model of anaemia induced by blood-loss in a time course study of 15 days. Haematological parameters and bone marrow cellularities were determined. Bone marrow apoptotic assays included: double fluorescent staining (acridine orange/ethidium bromide) and TUNEL. Bone marrow clonogenic assays were performed for evaluating erythroid colony forming unit?s expansion. The Erythropoietin receptor, Bax, Bcl-xL, Smac/DIABLO, caspase-3 and cytochrome c expressions were assessed by immunoblottings. Caspase-3 activity was determined with a colorimetric assay kit. Bleeding induces bone marrow apoptosis from 1 to 3 days, concomitant with Bax over-expression and Bcl-xL decrease. The mitochondrial dysfunction caused cytochrome c and Smac/DIABLO release to cytosol and caspase-3 activation. Erythropoietic recovery was associated with Erythropoietin receptor over expression from the third day, concomitant with the erythroid progenitors and Bcl-xL/Bax ratio enhancements. Erythropoiesis after bleeding depends on a delicate balance among proapoptotic (Bax, caspase-3, cytochrome c, Smac/DIABLO) and prosurvival proteins (Erythropoietin receptor, Bcl-xL), as the crucial regulators in bone marrow erythroid recovery. These findings provide new insights into the homeostatic mechanisms which promote erythropoietic response post-bleeding.Fil: Todaro, Juan Santiago. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; ArgentinaFil: Stoyanoff, Tania Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; Argentina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; ArgentinaFil: Aguirre, María Victoria. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; ArgentinaFil: Brandan, Nora Cristina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; ArgentinaScience Alert2013-04info: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/11336/77459Todaro, Juan Santiago; Stoyanoff, Tania Romina; Aguirre, María Victoria; Brandan, Nora Cristina; Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding; Science Alert; Journal of of Biological Sciences; 13; 6; 4-2013; 452-4621812-5719CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.scialert.net/abstract/?doi=jbs.2013.452.462info:eu-repo/semantics/altIdentifier/doi/10.3923/jbs.2013.452.462info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:25:21Zoai:ri.conicet.gov.ar:11336/77459instacron: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:34982025-10-15 14:25:21.41CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
title Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
spellingShingle Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
Todaro, Juan Santiago
Apoptosis
Bleeding
Bone Marrow
Caspase 3
Erythropoietin Receptor
title_short Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
title_full Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
title_fullStr Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
title_full_unstemmed Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
title_sort Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding
dc.creator.none.fl_str_mv Todaro, Juan Santiago
Stoyanoff, Tania Romina
Aguirre, María Victoria
Brandan, Nora Cristina
author Todaro, Juan Santiago
author_facet Todaro, Juan Santiago
Stoyanoff, Tania Romina
Aguirre, María Victoria
Brandan, Nora Cristina
author_role author
author2 Stoyanoff, Tania Romina
Aguirre, María Victoria
Brandan, Nora Cristina
author2_role author
author
author
dc.subject.none.fl_str_mv Apoptosis
Bleeding
Bone Marrow
Caspase 3
Erythropoietin Receptor
topic Apoptosis
Bleeding
Bone Marrow
Caspase 3
Erythropoietin Receptor
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The underlying interactions among apoptosis, erythroid proliferation and differentiation involved in bone marrow erythropoietic response after an acute blood-loss have not yet been elucidated in detail. We hypothesized that Erythropoietin receptor, Bax, caspase-3, cytochrome c, Smac/DIABLO and Bcl-xL molecules play important roles at time of acute erythropoietic need to ameliorate the hypoxic stress. Experiments were performed using in vivo murine model of anaemia induced by blood-loss in a time course study of 15 days. Haematological parameters and bone marrow cellularities were determined. Bone marrow apoptotic assays included: double fluorescent staining (acridine orange/ethidium bromide) and TUNEL. Bone marrow clonogenic assays were performed for evaluating erythroid colony forming unit?s expansion. The Erythropoietin receptor, Bax, Bcl-xL, Smac/DIABLO, caspase-3 and cytochrome c expressions were assessed by immunoblottings. Caspase-3 activity was determined with a colorimetric assay kit. Bleeding induces bone marrow apoptosis from 1 to 3 days, concomitant with Bax over-expression and Bcl-xL decrease. The mitochondrial dysfunction caused cytochrome c and Smac/DIABLO release to cytosol and caspase-3 activation. Erythropoietic recovery was associated with Erythropoietin receptor over expression from the third day, concomitant with the erythroid progenitors and Bcl-xL/Bax ratio enhancements. Erythropoiesis after bleeding depends on a delicate balance among proapoptotic (Bax, caspase-3, cytochrome c, Smac/DIABLO) and prosurvival proteins (Erythropoietin receptor, Bcl-xL), as the crucial regulators in bone marrow erythroid recovery. These findings provide new insights into the homeostatic mechanisms which promote erythropoietic response post-bleeding.
Fil: Todaro, Juan Santiago. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Stoyanoff, Tania Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; Argentina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Aguirre, María Victoria. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina
Fil: Brandan, Nora Cristina. Universidad Nacional del Nordeste. Facultad de Medicina. Cátedra de Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste; Argentina
description The underlying interactions among apoptosis, erythroid proliferation and differentiation involved in bone marrow erythropoietic response after an acute blood-loss have not yet been elucidated in detail. We hypothesized that Erythropoietin receptor, Bax, caspase-3, cytochrome c, Smac/DIABLO and Bcl-xL molecules play important roles at time of acute erythropoietic need to ameliorate the hypoxic stress. Experiments were performed using in vivo murine model of anaemia induced by blood-loss in a time course study of 15 days. Haematological parameters and bone marrow cellularities were determined. Bone marrow apoptotic assays included: double fluorescent staining (acridine orange/ethidium bromide) and TUNEL. Bone marrow clonogenic assays were performed for evaluating erythroid colony forming unit?s expansion. The Erythropoietin receptor, Bax, Bcl-xL, Smac/DIABLO, caspase-3 and cytochrome c expressions were assessed by immunoblottings. Caspase-3 activity was determined with a colorimetric assay kit. Bleeding induces bone marrow apoptosis from 1 to 3 days, concomitant with Bax over-expression and Bcl-xL decrease. The mitochondrial dysfunction caused cytochrome c and Smac/DIABLO release to cytosol and caspase-3 activation. Erythropoietic recovery was associated with Erythropoietin receptor over expression from the third day, concomitant with the erythroid progenitors and Bcl-xL/Bax ratio enhancements. Erythropoiesis after bleeding depends on a delicate balance among proapoptotic (Bax, caspase-3, cytochrome c, Smac/DIABLO) and prosurvival proteins (Erythropoietin receptor, Bcl-xL), as the crucial regulators in bone marrow erythroid recovery. These findings provide new insights into the homeostatic mechanisms which promote erythropoietic response post-bleeding.
publishDate 2013
dc.date.none.fl_str_mv 2013-04
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/11336/77459
Todaro, Juan Santiago; Stoyanoff, Tania Romina; Aguirre, María Victoria; Brandan, Nora Cristina; Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding; Science Alert; Journal of of Biological Sciences; 13; 6; 4-2013; 452-462
1812-5719
CONICET Digital
CONICET
url http://hdl.handle.net/11336/77459
identifier_str_mv Todaro, Juan Santiago; Stoyanoff, Tania Romina; Aguirre, María Victoria; Brandan, Nora Cristina; Molecular Mechanisms Involved in Murine Bone Marrow Erythropietic response to Acute Anaemia by Bleeding; Science Alert; Journal of of Biological Sciences; 13; 6; 4-2013; 452-462
1812-5719
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://www.scialert.net/abstract/?doi=jbs.2013.452.462
info:eu-repo/semantics/altIdentifier/doi/10.3923/jbs.2013.452.462
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 Science Alert
publisher.none.fl_str_mv Science Alert
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 13.22299

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