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dc.contributor.author
Danielczok, Jens
dc.contributor.author
Hertz, Laura
dc.contributor.author
Ruppenthal, Sandra
dc.contributor.author
Kaiser, Elisabeth
dc.contributor.author
Petkova Kirova, Polina
dc.contributor.author
Bogdanova, Anna
dc.contributor.author
Krause, Elmar
dc.contributor.author
Lipp, Peter
dc.contributor.author
Freichel, Marc
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Kaestner, Lars
dc.date.available
2018-06-08T15:05:51Z
dc.date.issued
2017-05
dc.identifier.citation
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
dc.identifier.issn
1015-8987
dc.identifier.uri
http://hdl.handle.net/11336/47860
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Karger
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Calcuim-Signalling
dc.subject
Erythropoietin
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Prostaglandin E2
dc.subject
Red Cells
dc.subject
Trpc Channels
dc.subject.classification
Inmunología
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Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Does Erythropoietin Regulate TRPC Channels in Red Blood Cells?
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-07T14:08:40Z
dc.journal.volume
41
dc.journal.number
3
dc.journal.pagination
1219-1228
dc.journal.pais
Suiza
dc.journal.ciudad
Basel
dc.description.fil
Fil: Danielczok, Jens. Universitat Saarland; Alemania
dc.description.fil
Fil: Hertz, Laura. Universitat Saarland; Alemania
dc.description.fil
Fil: Ruppenthal, Sandra. Universitat Saarland; Alemania
dc.description.fil
Fil: Kaiser, Elisabeth. Universitat Saarland; Alemania
dc.description.fil
Fil: Petkova Kirova, Polina. Universitat Saarland; Alemania
dc.description.fil
Fil: Bogdanova, Anna. Universitat Zurich; Suiza
dc.description.fil
Fil: Krause, Elmar. Universitat Saarland; Alemania
dc.description.fil
Fil: Lipp, Peter. Universitat Saarland; Alemania
dc.description.fil
Fil: Freichel, Marc. University Heidelberg; Alemania
dc.description.fil
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
dc.description.fil
Fil: Kaestner, Lars. Universitat Saarland; Alemania
dc.journal.title
Cellular Physiology and Biochemistry
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1159/000464384
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/464384
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