Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?

Autores
Danielczok, Jens; Hertz, Laura; Ruppenthal, Sandra; Kaiser, Elisabeth; Petkova Kirova, Polina; Bogdanova, Anna; Krause, Elmar; Lipp, Peter; Freichel, Marc; Birnbaumer, Lutz; Kaestner, Lars
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: Cation channels play an essential role in red blood cells (RBCs) ion homeostasis. One set of ion channels are the transient receptor potential channels of canonical type (TRPC channels). The abundance of these channels in primary erythroblasts, erythroid cell lines and RBCs was associated with an increase in intracellular Ca2+ upon stimulation with Erythropoietin (Epo). In contrast two independent studies on Epo-treated patients revealed diminished basal Ca2+ concentration or reduced phosphatidylserine exposure to the outer membrane leaflet. Methods: To resolve the seemingly conflicting reports we challenged mature human and mouse RBCs of several genotypes with Epo and Prostaglandin E2 (PGE2) and recorded the intracellular Ca2+ content. Next Generation Sequencing was utilised to approach a molecular analysis of reticulocytes. Results/Conclusions: Our results allow concluding that Epo and PGE2 regulation of the Ca2+ homeostasis is distinctly different between murine and human RBCs and that changes in intracellular Ca2+ upon Epo treatment is a primary rather than a compensatory effect. In human RBCs, Epo itself has no effect on Ca2+ fluxes but inhibits the PGE2-induced Ca2+ entry. In murine mature RBCs functional evidence indicates TRPC4/C5 mediated Ca2+ entry activated by Epo whereas PGE2 leads to a TRPC independent Ca2+ entry.
Fil: Danielczok, Jens. Universitat Saarland; Alemania
Fil: Hertz, Laura. Universitat Saarland; Alemania
Fil: Ruppenthal, Sandra. Universitat Saarland; Alemania
Fil: Kaiser, Elisabeth. Universitat Saarland; Alemania
Fil: Petkova Kirova, Polina. Universitat Saarland; Alemania
Fil: Bogdanova, Anna. Universitat Zurich; Suiza
Fil: Krause, Elmar. Universitat Saarland; Alemania
Fil: Lipp, Peter. Universitat Saarland; Alemania
Fil: Freichel, Marc. University Heidelberg; Alemania
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Research Triangle Park; Estados Unidos
Fil: Kaestner, Lars. Universitat Saarland; Alemania
Materia
CALCUIM-SIGNALLING
ERYTHROPOIETIN
PROSTAGLANDIN E2
RED CELLS
TRPC CHANNELS
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:11336/47860
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/47860
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?Danielczok, JensHertz, LauraRuppenthal, SandraKaiser, ElisabethPetkova Kirova, PolinaBogdanova, AnnaKrause, ElmarLipp, PeterFreichel, MarcBirnbaumer, LutzKaestner, LarsCALCUIM-SIGNALLINGERYTHROPOIETINPROSTAGLANDIN E2RED CELLSTRPC CHANNELShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: Cation channels play an essential role in red blood cells (RBCs) ion homeostasis. One set of ion channels are the transient receptor potential channels of canonical type (TRPC channels). The abundance of these channels in primary erythroblasts, erythroid cell lines and RBCs was associated with an increase in intracellular Ca2+ upon stimulation with Erythropoietin (Epo). In contrast two independent studies on Epo-treated patients revealed diminished basal Ca2+ concentration or reduced phosphatidylserine exposure to the outer membrane leaflet. Methods: To resolve the seemingly conflicting reports we challenged mature human and mouse RBCs of several genotypes with Epo and Prostaglandin E2 (PGE2) and recorded the intracellular Ca2+ content. Next Generation Sequencing was utilised to approach a molecular analysis of reticulocytes. Results/Conclusions: Our results allow concluding that Epo and PGE2 regulation of the Ca2+ homeostasis is distinctly different between murine and human RBCs and that changes in intracellular Ca2+ upon Epo treatment is a primary rather than a compensatory effect. In human RBCs, Epo itself has no effect on Ca2+ fluxes but inhibits the PGE2-induced Ca2+ entry. In murine mature RBCs functional evidence indicates TRPC4/C5 mediated Ca2+ entry activated by Epo whereas PGE2 leads to a TRPC independent Ca2+ entry.Fil: Danielczok, Jens. Universitat Saarland; AlemaniaFil: Hertz, Laura. Universitat Saarland; AlemaniaFil: Ruppenthal, Sandra. Universitat Saarland; AlemaniaFil: Kaiser, Elisabeth. Universitat Saarland; AlemaniaFil: Petkova Kirova, Polina. Universitat Saarland; AlemaniaFil: Bogdanova, Anna. Universitat Zurich; SuizaFil: Krause, Elmar. Universitat Saarland; AlemaniaFil: Lipp, Peter. Universitat Saarland; AlemaniaFil: Freichel, Marc. University Heidelberg; AlemaniaFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Research Triangle Park; Estados UnidosFil: Kaestner, Lars. Universitat Saarland; AlemaniaKarger2017-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47860Danielczok, Jens; Hertz, Laura; Ruppenthal, Sandra; Kaiser, Elisabeth; Petkova Kirova, Polina; et al.; Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?; Karger; Cellular Physiology and Biochemistry; 41; 3; 5-2017; 1219-12281015-8987CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1159/000464384info:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/464384info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:47:57Zoai:ri.conicet.gov.ar:11336/47860instacron: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 09:47:57.953CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
title Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
spellingShingle Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
Danielczok, Jens
CALCUIM-SIGNALLING
ERYTHROPOIETIN
PROSTAGLANDIN E2
RED CELLS
TRPC CHANNELS
title_short Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
title_full Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
title_fullStr Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
title_full_unstemmed Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
title_sort Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
dc.creator.none.fl_str_mv Danielczok, Jens
Hertz, Laura
Ruppenthal, Sandra
Kaiser, Elisabeth
Petkova Kirova, Polina
Bogdanova, Anna
Krause, Elmar
Lipp, Peter
Freichel, Marc
Birnbaumer, Lutz
Kaestner, Lars
author Danielczok, Jens
author_facet Danielczok, Jens
Hertz, Laura
Ruppenthal, Sandra
Kaiser, Elisabeth
Petkova Kirova, Polina
Bogdanova, Anna
Krause, Elmar
Lipp, Peter
Freichel, Marc
Birnbaumer, Lutz
Kaestner, Lars
author_role author
author2 Hertz, Laura
Ruppenthal, Sandra
Kaiser, Elisabeth
Petkova Kirova, Polina
Bogdanova, Anna
Krause, Elmar
Lipp, Peter
Freichel, Marc
Birnbaumer, Lutz
Kaestner, Lars
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CALCUIM-SIGNALLING
ERYTHROPOIETIN
PROSTAGLANDIN E2
RED CELLS
TRPC CHANNELS
topic CALCUIM-SIGNALLING
ERYTHROPOIETIN
PROSTAGLANDIN E2
RED CELLS
TRPC CHANNELS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background: Cation channels play an essential role in red blood cells (RBCs) ion homeostasis. One set of ion channels are the transient receptor potential channels of canonical type (TRPC channels). The abundance of these channels in primary erythroblasts, erythroid cell lines and RBCs was associated with an increase in intracellular Ca2+ upon stimulation with Erythropoietin (Epo). In contrast two independent studies on Epo-treated patients revealed diminished basal Ca2+ concentration or reduced phosphatidylserine exposure to the outer membrane leaflet. Methods: To resolve the seemingly conflicting reports we challenged mature human and mouse RBCs of several genotypes with Epo and Prostaglandin E2 (PGE2) and recorded the intracellular Ca2+ content. Next Generation Sequencing was utilised to approach a molecular analysis of reticulocytes. Results/Conclusions: Our results allow concluding that Epo and PGE2 regulation of the Ca2+ homeostasis is distinctly different between murine and human RBCs and that changes in intracellular Ca2+ upon Epo treatment is a primary rather than a compensatory effect. In human RBCs, Epo itself has no effect on Ca2+ fluxes but inhibits the PGE2-induced Ca2+ entry. In murine mature RBCs functional evidence indicates TRPC4/C5 mediated Ca2+ entry activated by Epo whereas PGE2 leads to a TRPC independent Ca2+ entry.
Fil: Danielczok, Jens. Universitat Saarland; Alemania
Fil: Hertz, Laura. Universitat Saarland; Alemania
Fil: Ruppenthal, Sandra. Universitat Saarland; Alemania
Fil: Kaiser, Elisabeth. Universitat Saarland; Alemania
Fil: Petkova Kirova, Polina. Universitat Saarland; Alemania
Fil: Bogdanova, Anna. Universitat Zurich; Suiza
Fil: Krause, Elmar. Universitat Saarland; Alemania
Fil: Lipp, Peter. Universitat Saarland; Alemania
Fil: Freichel, Marc. University Heidelberg; Alemania
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Research Triangle Park; Estados Unidos
Fil: Kaestner, Lars. Universitat Saarland; Alemania
description Background: Cation channels play an essential role in red blood cells (RBCs) ion homeostasis. One set of ion channels are the transient receptor potential channels of canonical type (TRPC channels). The abundance of these channels in primary erythroblasts, erythroid cell lines and RBCs was associated with an increase in intracellular Ca2+ upon stimulation with Erythropoietin (Epo). In contrast two independent studies on Epo-treated patients revealed diminished basal Ca2+ concentration or reduced phosphatidylserine exposure to the outer membrane leaflet. Methods: To resolve the seemingly conflicting reports we challenged mature human and mouse RBCs of several genotypes with Epo and Prostaglandin E2 (PGE2) and recorded the intracellular Ca2+ content. Next Generation Sequencing was utilised to approach a molecular analysis of reticulocytes. Results/Conclusions: Our results allow concluding that Epo and PGE2 regulation of the Ca2+ homeostasis is distinctly different between murine and human RBCs and that changes in intracellular Ca2+ upon Epo treatment is a primary rather than a compensatory effect. In human RBCs, Epo itself has no effect on Ca2+ fluxes but inhibits the PGE2-induced Ca2+ entry. In murine mature RBCs functional evidence indicates TRPC4/C5 mediated Ca2+ entry activated by Epo whereas PGE2 leads to a TRPC independent Ca2+ entry.
publishDate 2017
dc.date.none.fl_str_mv 2017-05
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/11336/47860
Danielczok, Jens; Hertz, Laura; Ruppenthal, Sandra; Kaiser, Elisabeth; Petkova Kirova, Polina; et al.; Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?; Karger; Cellular Physiology and Biochemistry; 41; 3; 5-2017; 1219-1228
1015-8987
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47860
identifier_str_mv Danielczok, Jens; Hertz, Laura; Ruppenthal, Sandra; Kaiser, Elisabeth; Petkova Kirova, Polina; et al.; Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?; Karger; Cellular Physiology and Biochemistry; 41; 3; 5-2017; 1219-1228
1015-8987
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1159/000464384
info:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/464384
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
dc.publisher.none.fl_str_mv Karger
publisher.none.fl_str_mv Karger
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 12.885934

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