The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma

Autores
Suares, Alejandra Carolina; Russo, Ana Josefa; Verstuyf, Annemieke; Boland, Ricardo Leopoldo; González Pardo, María Verónica
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
We have previously shown that 1a,25-dihydroxyvitamin D3 [1a,25(OH)2D3] and its less calcemic analogTX 527 induce apoptosis via caspase-3 activation in endothelial cells (SVEC) and endothelial cells transformedby the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, westudied whether intrinsic apoptotic pathway could be activated by changing the balance between antiand pro-apoptotic proteins. Time response qRT-PCR analysis demonstrated that the mRNA level ofanti-apoptotic gene Bcl-2 decreased after 12 h and increased after 48 h treatment with 1a,25(OH)2D3or TX 527 in SVEC and vGPCR cells, whereas its protein level remained unchanged through time.mRNA levels of pro-apoptotic gene Bax significantly increased only in SVEC after 24 and 48 h treatmentwith 1a,25(OH)2D3 and TX 527 although its protein levels remained unchanged in both cell lines. BimmRNA and protein levels increased in SVEC and vGPCR cells. Bim protein increase by 1a,25(OH)2D3and TX 527 was abolished when the expression of vitamin D receptor (VDR) was suppressed. On the otherhand, Bortezomib (0.25?1 nM), an inhibitor of NF-jB pathway highly activated in vGPCR cells, increasedBim protein levels and induced caspase-3 cleavage. Altogether, these results indicate that 1a,25(OH)2D3and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 in SVECand vGPCR cells. Moreover, this effect is mediated by VDR and involves NF-jB pathway inhibition invGPCR.
Fil: Suares, Alejandra Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Russo, Ana Josefa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Verstuyf, Annemieke. Katholikie Universiteit Leuven; Bélgica
Fil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: González Pardo, María Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Materia
Vitamin D
Apoptosis
Kaposi Sarcoma
Endothelial Cells
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/6334
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcomaSuares, Alejandra CarolinaRusso, Ana JosefaVerstuyf, AnnemiekeBoland, Ricardo LeopoldoGonzález Pardo, María VerónicaVitamin DApoptosisKaposi SarcomaEndothelial Cellshttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1We have previously shown that 1a,25-dihydroxyvitamin D3 [1a,25(OH)2D3] and its less calcemic analogTX 527 induce apoptosis via caspase-3 activation in endothelial cells (SVEC) and endothelial cells transformedby the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, westudied whether intrinsic apoptotic pathway could be activated by changing the balance between antiand pro-apoptotic proteins. Time response qRT-PCR analysis demonstrated that the mRNA level ofanti-apoptotic gene Bcl-2 decreased after 12 h and increased after 48 h treatment with 1a,25(OH)2D3or TX 527 in SVEC and vGPCR cells, whereas its protein level remained unchanged through time.mRNA levels of pro-apoptotic gene Bax significantly increased only in SVEC after 24 and 48 h treatmentwith 1a,25(OH)2D3 and TX 527 although its protein levels remained unchanged in both cell lines. BimmRNA and protein levels increased in SVEC and vGPCR cells. Bim protein increase by 1a,25(OH)2D3and TX 527 was abolished when the expression of vitamin D receptor (VDR) was suppressed. On the otherhand, Bortezomib (0.25?1 nM), an inhibitor of NF-jB pathway highly activated in vGPCR cells, increasedBim protein levels and induced caspase-3 cleavage. Altogether, these results indicate that 1a,25(OH)2D3and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 in SVECand vGPCR cells. Moreover, this effect is mediated by VDR and involves NF-jB pathway inhibition invGPCR.Fil: Suares, Alejandra Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Russo, Ana Josefa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Verstuyf, Annemieke. Katholikie Universiteit Leuven; BélgicaFil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: González Pardo, María Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaElsevier Science Inc2015-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/6334Suares, Alejandra Carolina; Russo, Ana Josefa; Verstuyf, Annemieke ; Boland, Ricardo Leopoldo; González Pardo, María Verónica; The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma; Elsevier Science Inc; Steroids; 102; 8-2015; 85-910039-128Xenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.steroids.2015.08.005info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0039128X15002196info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:04:04Zoai:ri.conicet.gov.ar:11336/6334instacron: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 10:04:04.413CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
title The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
spellingShingle The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
Suares, Alejandra Carolina
Vitamin D
Apoptosis
Kaposi Sarcoma
Endothelial Cells
title_short The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
title_full The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
title_fullStr The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
title_full_unstemmed The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
title_sort The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma
dc.creator.none.fl_str_mv Suares, Alejandra Carolina
Russo, Ana Josefa
Verstuyf, Annemieke
Boland, Ricardo Leopoldo
González Pardo, María Verónica
author Suares, Alejandra Carolina
author_facet Suares, Alejandra Carolina
Russo, Ana Josefa
Verstuyf, Annemieke
Boland, Ricardo Leopoldo
González Pardo, María Verónica
author_role author
author2 Russo, Ana Josefa
Verstuyf, Annemieke
Boland, Ricardo Leopoldo
González Pardo, María Verónica
author2_role author
author
author
author
dc.subject.none.fl_str_mv Vitamin D
Apoptosis
Kaposi Sarcoma
Endothelial Cells
topic Vitamin D
Apoptosis
Kaposi Sarcoma
Endothelial Cells
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv We have previously shown that 1a,25-dihydroxyvitamin D3 [1a,25(OH)2D3] and its less calcemic analogTX 527 induce apoptosis via caspase-3 activation in endothelial cells (SVEC) and endothelial cells transformedby the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, westudied whether intrinsic apoptotic pathway could be activated by changing the balance between antiand pro-apoptotic proteins. Time response qRT-PCR analysis demonstrated that the mRNA level ofanti-apoptotic gene Bcl-2 decreased after 12 h and increased after 48 h treatment with 1a,25(OH)2D3or TX 527 in SVEC and vGPCR cells, whereas its protein level remained unchanged through time.mRNA levels of pro-apoptotic gene Bax significantly increased only in SVEC after 24 and 48 h treatmentwith 1a,25(OH)2D3 and TX 527 although its protein levels remained unchanged in both cell lines. BimmRNA and protein levels increased in SVEC and vGPCR cells. Bim protein increase by 1a,25(OH)2D3and TX 527 was abolished when the expression of vitamin D receptor (VDR) was suppressed. On the otherhand, Bortezomib (0.25?1 nM), an inhibitor of NF-jB pathway highly activated in vGPCR cells, increasedBim protein levels and induced caspase-3 cleavage. Altogether, these results indicate that 1a,25(OH)2D3and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 in SVECand vGPCR cells. Moreover, this effect is mediated by VDR and involves NF-jB pathway inhibition invGPCR.
Fil: Suares, Alejandra Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Russo, Ana Josefa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Verstuyf, Annemieke. Katholikie Universiteit Leuven; Bélgica
Fil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: González Pardo, María Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
description We have previously shown that 1a,25-dihydroxyvitamin D3 [1a,25(OH)2D3] and its less calcemic analogTX 527 induce apoptosis via caspase-3 activation in endothelial cells (SVEC) and endothelial cells transformedby the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR). In this work, westudied whether intrinsic apoptotic pathway could be activated by changing the balance between antiand pro-apoptotic proteins. Time response qRT-PCR analysis demonstrated that the mRNA level ofanti-apoptotic gene Bcl-2 decreased after 12 h and increased after 48 h treatment with 1a,25(OH)2D3or TX 527 in SVEC and vGPCR cells, whereas its protein level remained unchanged through time.mRNA levels of pro-apoptotic gene Bax significantly increased only in SVEC after 24 and 48 h treatmentwith 1a,25(OH)2D3 and TX 527 although its protein levels remained unchanged in both cell lines. BimmRNA and protein levels increased in SVEC and vGPCR cells. Bim protein increase by 1a,25(OH)2D3and TX 527 was abolished when the expression of vitamin D receptor (VDR) was suppressed. On the otherhand, Bortezomib (0.25?1 nM), an inhibitor of NF-jB pathway highly activated in vGPCR cells, increasedBim protein levels and induced caspase-3 cleavage. Altogether, these results indicate that 1a,25(OH)2D3and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 in SVECand vGPCR cells. Moreover, this effect is mediated by VDR and involves NF-jB pathway inhibition invGPCR.
publishDate 2015
dc.date.none.fl_str_mv 2015-08
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/11336/6334
Suares, Alejandra Carolina; Russo, Ana Josefa; Verstuyf, Annemieke ; Boland, Ricardo Leopoldo; González Pardo, María Verónica; The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma; Elsevier Science Inc; Steroids; 102; 8-2015; 85-91
0039-128X
url http://hdl.handle.net/11336/6334
identifier_str_mv Suares, Alejandra Carolina; Russo, Ana Josefa; Verstuyf, Annemieke ; Boland, Ricardo Leopoldo; González Pardo, María Verónica; The proapoptotic protein Bim is up regulated by 1α,25-dihydroxyvitamin D3 and its receptor agonist in endothelial cells and transformed by viral GPCR associated to Kaposi sarcoma; Elsevier Science Inc; Steroids; 102; 8-2015; 85-91
0039-128X
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.steroids.2015.08.005
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0039128X15002196
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science Inc
publisher.none.fl_str_mv Elsevier Science Inc
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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