α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR

Autores
Tapia, Cinthya Mariela; Uranga, Romina Maria; Salvador, Gabriela Alejandra; González Pardo, Verónica
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
The infectious cause of Kaposi’s sarcoma (KS) neoplasm is KS-associated Herpesvirus (KSHV or human herpesvirus 8). Furthermore, virally G Protein-coupled Receptor (vGPCR) is one of the molecules from the lytic phase able to induce KS associated cellular modifications through paracrine oncogenesis. We have previously demonstrated that 1α,25(OH)2D3 exerts antiproliferative effects on endothelial cells that stably express vGPCR by inhibiting NF-κB pathway and promoting apoptosis and autophagy. Oxidative stress is frequent in many types of cancer where reactive oxygen species (ROS) can act as a promoting or suppressing agent. In this work, our goal was to study the involvement of ROS as part of the antineoplastic mechanisms triggered by 1α,25(OH)2D3 in vGPCR cells. By a spectrofluorimetric method using the H2-DCF-DA probe, ROS levels were detected higher than control conditions after 1α,25(OH)2D3 (10 nM, 24 or 48 h) treatment. When VDR expression was knocked down by shRNA against VDR (vGPCR-shVDR cell line), ROS increase was found to be VDR dependent (48 h). Our previous reports indicated that vGPCR cells proliferation decreases at 80% after 1α,25(OH)2D3 treatment, triggering cell cycle arrest and apoptosis by a mechanism dependent on the caspase-3 cleavage. In this case, Western blot studies showed an increase expression of pro-apoptotic proteins like BIM and caspase-3 cleavage by 1α,25(OH)2D3 (10 nM, 48 h) and no reversal effect by N-Acetyl-cysteine (1 mM) antioxidant was observed. Altogether, these preliminary results suggest that ROS levels promotion by 1α,25(OH)2D3 through VDR, triggers apoptosis-related mechanisms on vGPCR cells.
Fil: Tapia, Cinthya Mariela. 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: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: González Pardo, 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
LV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología General
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Sociedad Argentina de Microbiología general
Materia
OXIDATIVE STRESS
vGPCR
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:11336/159595
Acceder
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network_name_str CONICET Digital (CONICET)
spelling α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCRTapia, Cinthya MarielaUranga, Romina MariaSalvador, Gabriela AlejandraGonzález Pardo, VerónicaOXIDATIVE STRESSvGPCRhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The infectious cause of Kaposi’s sarcoma (KS) neoplasm is KS-associated Herpesvirus (KSHV or human herpesvirus 8). Furthermore, virally G Protein-coupled Receptor (vGPCR) is one of the molecules from the lytic phase able to induce KS associated cellular modifications through paracrine oncogenesis. We have previously demonstrated that 1α,25(OH)2D3 exerts antiproliferative effects on endothelial cells that stably express vGPCR by inhibiting NF-κB pathway and promoting apoptosis and autophagy. Oxidative stress is frequent in many types of cancer where reactive oxygen species (ROS) can act as a promoting or suppressing agent. In this work, our goal was to study the involvement of ROS as part of the antineoplastic mechanisms triggered by 1α,25(OH)2D3 in vGPCR cells. By a spectrofluorimetric method using the H2-DCF-DA probe, ROS levels were detected higher than control conditions after 1α,25(OH)2D3 (10 nM, 24 or 48 h) treatment. When VDR expression was knocked down by shRNA against VDR (vGPCR-shVDR cell line), ROS increase was found to be VDR dependent (48 h). Our previous reports indicated that vGPCR cells proliferation decreases at 80% after 1α,25(OH)2D3 treatment, triggering cell cycle arrest and apoptosis by a mechanism dependent on the caspase-3 cleavage. In this case, Western blot studies showed an increase expression of pro-apoptotic proteins like BIM and caspase-3 cleavage by 1α,25(OH)2D3 (10 nM, 48 h) and no reversal effect by N-Acetyl-cysteine (1 mM) antioxidant was observed. Altogether, these preliminary results suggest that ROS levels promotion by 1α,25(OH)2D3 through VDR, triggers apoptosis-related mechanisms on vGPCR cells.Fil: Tapia, Cinthya Mariela. 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: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: González Pardo, 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; ArgentinaLV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología GeneralArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularSociedad Argentina de Microbiología generalTech Science Press2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentapplication/pdfhttp://hdl.handle.net/11336/159595α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR; LV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología General; Argentina; 2020; 138-1380327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.saib.org.ar/index.php?q=node/562Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:02:18Zoai:ri.conicet.gov.ar:11336/159595instacron: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 15:02:18.575CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
title α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
spellingShingle α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
Tapia, Cinthya Mariela
OXIDATIVE STRESS
vGPCR
title_short α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
title_full α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
title_fullStr α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
title_full_unstemmed α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
title_sort α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR
dc.creator.none.fl_str_mv Tapia, Cinthya Mariela
Uranga, Romina Maria
Salvador, Gabriela Alejandra
González Pardo, Verónica
author Tapia, Cinthya Mariela
author_facet Tapia, Cinthya Mariela
Uranga, Romina Maria
Salvador, Gabriela Alejandra
González Pardo, Verónica
author_role author
author2 Uranga, Romina Maria
Salvador, Gabriela Alejandra
González Pardo, Verónica
author2_role author
author
author
dc.subject.none.fl_str_mv OXIDATIVE STRESS
vGPCR
topic OXIDATIVE STRESS
vGPCR
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The infectious cause of Kaposi’s sarcoma (KS) neoplasm is KS-associated Herpesvirus (KSHV or human herpesvirus 8). Furthermore, virally G Protein-coupled Receptor (vGPCR) is one of the molecules from the lytic phase able to induce KS associated cellular modifications through paracrine oncogenesis. We have previously demonstrated that 1α,25(OH)2D3 exerts antiproliferative effects on endothelial cells that stably express vGPCR by inhibiting NF-κB pathway and promoting apoptosis and autophagy. Oxidative stress is frequent in many types of cancer where reactive oxygen species (ROS) can act as a promoting or suppressing agent. In this work, our goal was to study the involvement of ROS as part of the antineoplastic mechanisms triggered by 1α,25(OH)2D3 in vGPCR cells. By a spectrofluorimetric method using the H2-DCF-DA probe, ROS levels were detected higher than control conditions after 1α,25(OH)2D3 (10 nM, 24 or 48 h) treatment. When VDR expression was knocked down by shRNA against VDR (vGPCR-shVDR cell line), ROS increase was found to be VDR dependent (48 h). Our previous reports indicated that vGPCR cells proliferation decreases at 80% after 1α,25(OH)2D3 treatment, triggering cell cycle arrest and apoptosis by a mechanism dependent on the caspase-3 cleavage. In this case, Western blot studies showed an increase expression of pro-apoptotic proteins like BIM and caspase-3 cleavage by 1α,25(OH)2D3 (10 nM, 48 h) and no reversal effect by N-Acetyl-cysteine (1 mM) antioxidant was observed. Altogether, these preliminary results suggest that ROS levels promotion by 1α,25(OH)2D3 through VDR, triggers apoptosis-related mechanisms on vGPCR cells.
Fil: Tapia, Cinthya Mariela. 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: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: González Pardo, 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
LV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología General
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Sociedad Argentina de Microbiología general
description The infectious cause of Kaposi’s sarcoma (KS) neoplasm is KS-associated Herpesvirus (KSHV or human herpesvirus 8). Furthermore, virally G Protein-coupled Receptor (vGPCR) is one of the molecules from the lytic phase able to induce KS associated cellular modifications through paracrine oncogenesis. We have previously demonstrated that 1α,25(OH)2D3 exerts antiproliferative effects on endothelial cells that stably express vGPCR by inhibiting NF-κB pathway and promoting apoptosis and autophagy. Oxidative stress is frequent in many types of cancer where reactive oxygen species (ROS) can act as a promoting or suppressing agent. In this work, our goal was to study the involvement of ROS as part of the antineoplastic mechanisms triggered by 1α,25(OH)2D3 in vGPCR cells. By a spectrofluorimetric method using the H2-DCF-DA probe, ROS levels were detected higher than control conditions after 1α,25(OH)2D3 (10 nM, 24 or 48 h) treatment. When VDR expression was knocked down by shRNA against VDR (vGPCR-shVDR cell line), ROS increase was found to be VDR dependent (48 h). Our previous reports indicated that vGPCR cells proliferation decreases at 80% after 1α,25(OH)2D3 treatment, triggering cell cycle arrest and apoptosis by a mechanism dependent on the caspase-3 cleavage. In this case, Western blot studies showed an increase expression of pro-apoptotic proteins like BIM and caspase-3 cleavage by 1α,25(OH)2D3 (10 nM, 48 h) and no reversal effect by N-Acetyl-cysteine (1 mM) antioxidant was observed. Altogether, these preliminary results suggest that ROS levels promotion by 1α,25(OH)2D3 through VDR, triggers apoptosis-related mechanisms on vGPCR cells.
publishDate 2020
dc.date.none.fl_str_mv 2020
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dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/159595
α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR; LV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología General; Argentina; 2020; 138-138
0327-9545
1667-5746
CONICET Digital
CONICET
url http://hdl.handle.net/11336/159595
identifier_str_mv α,25(OH)2D3 Promotes oxidative stress in endothelial cells transformed by vGPCR; LV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular y XV Reunión Anual de la Sociedad Argentina de Microbiología General; Argentina; 2020; 138-138
0327-9545
1667-5746
CONICET Digital
CONICET
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language eng
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