Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic dru...
- Autores
- Asuaje, Agustín; Martín, Pedro; Enrique, Nicolás Jorge; Diaz Zegarra, Leandro Agustín; Smaldini, Paola Lorena; Docena, Guillermo Horacio; Milesi, Verónica
- Año de publicación
- 2018
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- An established characteristic of neoplastic cells is their metabolic reprogramming, known as the Warburg effect, with greater reliance on energetically less efficient pathways (such as glycolysis and pentose phosphate shunt) compared with oxidative phosphorylation. This results in an overproduction of acidic species that must be extruded to maintain intracellular homeostasis. We recently described that blocking the proton currents in leukemic cells mediated by Hv1 ion channels triggers a marked intracellular acidification and apoptosis induction. Moreover, histamine H1-receptor antagonists were found to induce apoptosis in tumoral cells but the mechanism is still unclear. By using Jurkat T cells, we now show how diphenhydramine inhibits Hv1 mediated currents, inducing a drop in intracellular pH and cellular viability. This provides evidence of a new target structure responsible of the known pro-apoptotic action of antihistaminic drugs.
Facultad de Ciencias Exactas
Instituto de Estudios Inmunológicos y Fisiopatológicos - Materia
-
Ciencias Exactas
Ciencias Médicas
antihistaminic
Apoptosis
cancer
diphenhydramine
HVCN1
intracellular pH
leukemia
proton channels - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/107777
Ver los metadatos del registro completo
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Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugsAsuaje, AgustínMartín, PedroEnrique, Nicolás JorgeDiaz Zegarra, Leandro AgustínSmaldini, Paola LorenaDocena, Guillermo HoracioMilesi, VerónicaCiencias ExactasCiencias MédicasantihistaminicApoptosiscancerdiphenhydramineHVCN1intracellular pHleukemiaproton channelsAn established characteristic of neoplastic cells is their metabolic reprogramming, known as the Warburg effect, with greater reliance on energetically less efficient pathways (such as glycolysis and pentose phosphate shunt) compared with oxidative phosphorylation. This results in an overproduction of acidic species that must be extruded to maintain intracellular homeostasis. We recently described that blocking the proton currents in leukemic cells mediated by Hv1 ion channels triggers a marked intracellular acidification and apoptosis induction. Moreover, histamine H1-receptor antagonists were found to induce apoptosis in tumoral cells but the mechanism is still unclear. By using Jurkat T cells, we now show how diphenhydramine inhibits Hv1 mediated currents, inducing a drop in intracellular pH and cellular viability. This provides evidence of a new target structure responsible of the known pro-apoptotic action of antihistaminic drugs.Facultad de Ciencias ExactasInstituto de Estudios Inmunológicos y Fisiopatológicos2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf58-64http://sedici.unlp.edu.ar/handle/10915/107777enginfo:eu-repo/semantics/altIdentifier/url/http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5972794&blobtype=pdfinfo:eu-repo/semantics/altIdentifier/url/https://www.tandfonline.com/doi/full/10.1080/19336950.2017.1331799info:eu-repo/semantics/altIdentifier/issn/1933-6969info:eu-repo/semantics/altIdentifier/pmid/28514187info:eu-repo/semantics/altIdentifier/doi/10.1080/19336950.2017.1331799info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:23:51Zoai:sedici.unlp.edu.ar:10915/107777Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:23:52.074SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
title |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
spellingShingle |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs Asuaje, Agustín Ciencias Exactas Ciencias Médicas antihistaminic Apoptosis cancer diphenhydramine HVCN1 intracellular pH leukemia proton channels |
title_short |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
title_full |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
title_fullStr |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
title_full_unstemmed |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
title_sort |
Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells- New insights into the pro-apoptotic effects of antihistaminic drugs |
dc.creator.none.fl_str_mv |
Asuaje, Agustín Martín, Pedro Enrique, Nicolás Jorge Diaz Zegarra, Leandro Agustín Smaldini, Paola Lorena Docena, Guillermo Horacio Milesi, Verónica |
author |
Asuaje, Agustín |
author_facet |
Asuaje, Agustín Martín, Pedro Enrique, Nicolás Jorge Diaz Zegarra, Leandro Agustín Smaldini, Paola Lorena Docena, Guillermo Horacio Milesi, Verónica |
author_role |
author |
author2 |
Martín, Pedro Enrique, Nicolás Jorge Diaz Zegarra, Leandro Agustín Smaldini, Paola Lorena Docena, Guillermo Horacio Milesi, Verónica |
author2_role |
author author author author author author |
dc.subject.none.fl_str_mv |
Ciencias Exactas Ciencias Médicas antihistaminic Apoptosis cancer diphenhydramine HVCN1 intracellular pH leukemia proton channels |
topic |
Ciencias Exactas Ciencias Médicas antihistaminic Apoptosis cancer diphenhydramine HVCN1 intracellular pH leukemia proton channels |
dc.description.none.fl_txt_mv |
An established characteristic of neoplastic cells is their metabolic reprogramming, known as the Warburg effect, with greater reliance on energetically less efficient pathways (such as glycolysis and pentose phosphate shunt) compared with oxidative phosphorylation. This results in an overproduction of acidic species that must be extruded to maintain intracellular homeostasis. We recently described that blocking the proton currents in leukemic cells mediated by Hv1 ion channels triggers a marked intracellular acidification and apoptosis induction. Moreover, histamine H1-receptor antagonists were found to induce apoptosis in tumoral cells but the mechanism is still unclear. By using Jurkat T cells, we now show how diphenhydramine inhibits Hv1 mediated currents, inducing a drop in intracellular pH and cellular viability. This provides evidence of a new target structure responsible of the known pro-apoptotic action of antihistaminic drugs. Facultad de Ciencias Exactas Instituto de Estudios Inmunológicos y Fisiopatológicos |
description |
An established characteristic of neoplastic cells is their metabolic reprogramming, known as the Warburg effect, with greater reliance on energetically less efficient pathways (such as glycolysis and pentose phosphate shunt) compared with oxidative phosphorylation. This results in an overproduction of acidic species that must be extruded to maintain intracellular homeostasis. We recently described that blocking the proton currents in leukemic cells mediated by Hv1 ion channels triggers a marked intracellular acidification and apoptosis induction. Moreover, histamine H1-receptor antagonists were found to induce apoptosis in tumoral cells but the mechanism is still unclear. By using Jurkat T cells, we now show how diphenhydramine inhibits Hv1 mediated currents, inducing a drop in intracellular pH and cellular viability. This provides evidence of a new target structure responsible of the known pro-apoptotic action of antihistaminic drugs. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo 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://sedici.unlp.edu.ar/handle/10915/107777 |
url |
http://sedici.unlp.edu.ar/handle/10915/107777 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5972794&blobtype=pdf info:eu-repo/semantics/altIdentifier/url/https://www.tandfonline.com/doi/full/10.1080/19336950.2017.1331799 info:eu-repo/semantics/altIdentifier/issn/1933-6969 info:eu-repo/semantics/altIdentifier/pmid/28514187 info:eu-repo/semantics/altIdentifier/doi/10.1080/19336950.2017.1331799 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
dc.format.none.fl_str_mv |
application/pdf 58-64 |
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SEDICI (UNLP) - Universidad Nacional de La Plata |
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