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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2018
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01719335_v97_n6_p411_Maltaneri http://hdl.handle.net/20.500.12110/paper_01719335_v97_n6_p411_Maltaneri |
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paper:paper_01719335_v97_n6_p411_Maltaneri2023-06-08T15:18:44Z Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration Amlodipine Angiogenesis Calcium channels Diltiazem Erythropoietin amlodipine blocking antibody calcium channel diltiazem erythropoietin reactive oxygen metabolite transient receptor potential channel 3 tumor necrosis factor calcium channel erythropoietin angiogenesis angiogenesis assay antiangiogenic activity Article calcium cell level calcium transport cell migration endothelium cell human human cell human cell culture in vitro study membrane channel priority journal umbilical vein endothelial cell cell culture cell membrane cell motion cytology endothelium cell metabolism Calcium Channels Cell Membrane Cell Movement Cells, Cultured Endothelial Cells Erythropoietin Humans 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 2018 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01719335_v97_n6_p411_Maltaneri http://hdl.handle.net/20.500.12110/paper_01719335_v97_n6_p411_Maltaneri |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Amlodipine Angiogenesis Calcium channels Diltiazem Erythropoietin amlodipine blocking antibody calcium channel diltiazem erythropoietin reactive oxygen metabolite transient receptor potential channel 3 tumor necrosis factor calcium channel erythropoietin angiogenesis angiogenesis assay antiangiogenic activity Article calcium cell level calcium transport cell migration endothelium cell human human cell human cell culture in vitro study membrane channel priority journal umbilical vein endothelial cell cell culture cell membrane cell motion cytology endothelium cell metabolism Calcium Channels Cell Membrane Cell Movement Cells, Cultured Endothelial Cells Erythropoietin Humans |
| spellingShingle |
Amlodipine Angiogenesis Calcium channels Diltiazem Erythropoietin amlodipine blocking antibody calcium channel diltiazem erythropoietin reactive oxygen metabolite transient receptor potential channel 3 tumor necrosis factor calcium channel erythropoietin angiogenesis angiogenesis assay antiangiogenic activity Article calcium cell level calcium transport cell migration endothelium cell human human cell human cell culture in vitro study membrane channel priority journal umbilical vein endothelial cell cell culture cell membrane cell motion cytology endothelium cell metabolism Calcium Channels Cell Membrane Cell Movement Cells, Cultured Endothelial Cells Erythropoietin Humans Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| topic_facet |
Amlodipine Angiogenesis Calcium channels Diltiazem Erythropoietin amlodipine blocking antibody calcium channel diltiazem erythropoietin reactive oxygen metabolite transient receptor potential channel 3 tumor necrosis factor calcium channel erythropoietin angiogenesis angiogenesis assay antiangiogenic activity Article calcium cell level calcium transport cell migration endothelium cell human human cell human cell culture in vitro study membrane channel priority journal umbilical vein endothelial cell cell culture cell membrane cell motion cytology endothelium cell metabolism Calcium Channels Cell Membrane Cell Movement Cells, Cultured Endothelial Cells Erythropoietin Humans |
| description |
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 |
| title |
Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| title_short |
Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| title_full |
Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| title_fullStr |
Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| title_full_unstemmed |
Participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| title_sort |
participation of membrane calcium channels in erythropoietin-induced endothelial cell migration |
| publishDate |
2018 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01719335_v97_n6_p411_Maltaneri http://hdl.handle.net/20.500.12110/paper_01719335_v97_n6_p411_Maltaneri |
| _version_ |
1768542216359247872 |