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, María Verónica
- Año de publicación
- 2021
- 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, 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
LVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General Microbiology
Argentina
Sociedad Argentina de Investigación Bioquímica
Asociación Civil de Microbiología General - Materia
-
OXIDATIVE STRESS
VITAMIN D
APOPTOSIS
TUMOR CELLS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/156497
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α,25(OH)2D3 promotes oxidative stress in endothelial cells transformed by vGPCRTapia, Cinthya MarielaUranga, Romina MariaSalvador, Gabriela AlejandraGonzález Pardo, María VerónicaOXIDATIVE STRESSVITAMIN DAPOPTOSISTUMOR CELLShttps://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, 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; ArgentinaLVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General MicrobiologyArgentinaSociedad Argentina de Investigación BioquímicaAsociación Civil de Microbiología GeneralTech Science Press2021info: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/11336/156497α,25(OH)2D3 promotes oxidative stress in endothelial cells transformed by vGPCR; LVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General Microbiology; Argentina; 2020; 1-1730327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.techscience.com/biocell/v45nSuppl.1Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:48:46Zoai:ri.conicet.gov.ar:11336/156497instacron: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:34982025-09-29 09:48:46.966CONICET 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 VITAMIN D APOPTOSIS TUMOR CELLS |
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, María Verónica |
author |
Tapia, Cinthya Mariela |
author_facet |
Tapia, Cinthya Mariela Uranga, Romina Maria Salvador, Gabriela Alejandra González Pardo, María Verónica |
author_role |
author |
author2 |
Uranga, Romina Maria Salvador, Gabriela Alejandra González Pardo, María Verónica |
author2_role |
author author author |
dc.subject.none.fl_str_mv |
OXIDATIVE STRESS VITAMIN D APOPTOSIS TUMOR CELLS |
topic |
OXIDATIVE STRESS VITAMIN D APOPTOSIS TUMOR 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 |
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, 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 LVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General Microbiology Argentina Sociedad Argentina de Investigación Bioquímica Asociación Civil 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 |
2021 |
dc.date.none.fl_str_mv |
2021 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/conferenceObject Reunión Journal http://purl.org/coar/resource_type/c_5794 info:ar-repo/semantics/documentoDeConferencia |
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publishedVersion |
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conferenceObject |
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http://hdl.handle.net/11336/156497 α,25(OH)2D3 promotes oxidative stress in endothelial cells transformed by vGPCR; LVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General Microbiology; Argentina; 2020; 1-173 0327-9545 1667-5746 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/156497 |
identifier_str_mv |
α,25(OH)2D3 promotes oxidative stress in endothelial cells transformed by vGPCR; LVI Annual Meeting Argentine Society for Biochemistry and Molecular Biology and XV Annual Meeting Argentinean Society for General Microbiology; Argentina; 2020; 1-173 0327-9545 1667-5746 CONICET Digital CONICET |
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eng |
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eng |
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Tech Science Press |
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Tech Science Press |
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