Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration

Calcium (Ca2+) plays an important role in angiogenesis, as it activates the cell migration machinery. Different proangiogenic factors have been demonstrated to induce transient Ca2+ increases in endothelial cells. This has raised interest in the contribution of Ca2+ channels to cell migration, and i...

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Autor principal: Maltaneri, R.E
Otros Autores: Schiappacasse, A., Chamorro, M.E, Nesse, A.B, Vittori, D.C
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Elsevier GmbH 2018
Acceso en línea:Registro en Scopus
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024 7 |2 cas  |a amlodipine, 88150-42-9, 103129-82-4, 736178-83-9; diltiazem, 33286-22-5, 42399-41-7; erythropoietin, 11096-26-7; Calcium Channels; Erythropoietin 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a EJCBD 
100 1 |a Maltaneri, R.E. 
245 1 0 |a Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration 
260 |b Elsevier GmbH  |c 2018 
270 1 0 |m Vittori, D.C.; Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón II, Piso 4, Ciudad Universitaria, Ciudad Autónoma de Buenos AiresArgentina; email: dvittori@qb.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a Calcium (Ca2+) plays an important role in angiogenesis, as it activates the cell migration machinery. Different proangiogenic factors have been demonstrated to induce transient Ca2+ increases in endothelial cells. This has raised interest in the contribution of Ca2+ channels to cell migration, and in a possible use of channel-blocking compounds in angiogenesis-related pathologies. We have investigated the ability of erythropoietin (Epo), a cytokine recently involved in angiogenesis, to induce Ca2+ influx through different types of membrane channels in EA.hy926 endothelial cells. The voltage-dependent Ca2+ channel antagonists amlodipine and diltiazem inhibited an Epo-triggered transient rise in intracellular Ca2+, similarly to a specific inhibitor (Pyr3) and a blocking antibody against the transient potential calcium channel 3 (TRPC3). Unlike diltiazem, amlodipine and the TRPC3 inhibitors prevented the stimulating action of Epo in cell migration and in vitro angiogenesis assays. Amlodipine was also able to inhibit an increase in endothelial cell migration induced by Epo in an inflammatory environment generated with TNF-α. These results support the participation of Ca2+ entry through voltage-dependent and transient potential channels in Epo-driven endothelial cell migration, highlighting the antiangiogenic activity of amlodipine. © 2018 Elsevier GmbH  |l eng 
536 |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica, ANPCYT-PICT 13-0692 
536 |a Detalles de la financiación: Universidad de Buenos Aires, UBACYT 200201301100246BA 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET 11220150100804CO 
536 |a Detalles de la financiación: This work was supported by the Universidad de Buenos Aires (UBACYT 200201301100246BA ), the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET 11220150100804CO ) and the Agencia Nacional de Promoción Científica y Tecnológica (ANPCYT-PICT 13-0692 ). Dr. Alcira Nesse, Dr. Daniela Vittori and Dr. María E. Chamorro are research scientists at the CONICET, and Dr. Romina Maltaneri and Lic. Agustina Schiappacasse have received fellowships from the CONICET (Argentina). 
593 |a Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto del Departamento de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN), Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Buenos Aires, Argentina 
690 1 0 |a AMLODIPINE 
690 1 0 |a ANGIOGENESIS 
690 1 0 |a CALCIUM CHANNELS 
690 1 0 |a DILTIAZEM 
690 1 0 |a ERYTHROPOIETIN 
690 1 0 |a AMLODIPINE 
690 1 0 |a BLOCKING ANTIBODY 
690 1 0 |a CALCIUM CHANNEL 
690 1 0 |a DILTIAZEM 
690 1 0 |a ERYTHROPOIETIN 
690 1 0 |a REACTIVE OXYGEN METABOLITE 
690 1 0 |a TRANSIENT RECEPTOR POTENTIAL CHANNEL 3 
690 1 0 |a TUMOR NECROSIS FACTOR 
690 1 0 |a CALCIUM CHANNEL 
690 1 0 |a ERYTHROPOIETIN 
690 1 0 |a ANGIOGENESIS 
690 1 0 |a ANGIOGENESIS ASSAY 
690 1 0 |a ANTIANGIOGENIC ACTIVITY 
690 1 0 |a ARTICLE 
690 1 0 |a CALCIUM CELL LEVEL 
690 1 0 |a CALCIUM TRANSPORT 
690 1 0 |a CELL MIGRATION 
690 1 0 |a ENDOTHELIUM CELL 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a HUMAN CELL CULTURE 
690 1 0 |a IN VITRO STUDY 
690 1 0 |a MEMBRANE CHANNEL 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a UMBILICAL VEIN ENDOTHELIAL CELL 
690 1 0 |a CELL CULTURE 
690 1 0 |a CELL MEMBRANE 
690 1 0 |a CELL MOTION 
690 1 0 |a CYTOLOGY 
690 1 0 |a ENDOTHELIUM CELL 
690 1 0 |a METABOLISM 
690 1 0 |a CALCIUM CHANNELS 
690 1 0 |a CELL MEMBRANE 
690 1 0 |a CELL MOVEMENT 
690 1 0 |a CELLS, CULTURED 
690 1 0 |a ENDOTHELIAL CELLS 
690 1 0 |a ERYTHROPOIETIN 
690 1 0 |a HUMANS 
700 1 |a Schiappacasse, A. 
700 1 |a Chamorro, M.E. 
700 1 |a Nesse, A.B. 
700 1 |a Vittori, D.C. 
773 0 |d Elsevier GmbH, 2018  |g v. 97  |h pp. 411-421  |k n. 6  |p Eur. J. Cell Biol.  |x 01719335  |t European Journal of Cell Biology 
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856 4 0 |u https://doi.org/10.1016/j.ejcb.2018.06.002  |y DOI 
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