Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors
- Autores
- Etulain, Julia; Negrotto, Soledad; Tribulatti, María Virginia; Croci, Diego Omar; Carabelli, Julieta; Campetella, Oscar Eduardo; Rabinovich, Gabriel Adrián; Schattner, Mirta Ana
- Año de publicación
- 2014
- Idioma
- español castellano
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Platelets contribute to vessel formation through the release of angiogenesis-modulating factors stored in their α-granules. Galectins, a family of lectins that bind β-galactoside residues, are up-regulated in inflammatory and cancerous tissues, trigger platelet activation and mediate vascularization processes. Here we aimed to elucidate whether the release of platelet-derived proangiogenic molecules could represent an alternative mechanism through which galectins promote neovascularization. We show that different members of the galectin family can selectively regulate the release of angiogenic molecules by human platelets. Whereas Galectin (Gal)-1, -3, and -8 triggered vascular endothelial growth factor (VEGF) release, only Gal-8 induced endostatin secretion. Release of VEGF induced by Gal-8 was partially prevented by COX-1, PKC, p38 and Src kinases inhibitors, whereas Gal-1-induced VEGF secretion was inhibited by PKC and ERK blockade, and Gal-3 triggered VEGF release selectively through a PKC-dependent pathway. Regarding endostatin, Gal-8 failed to stimulate its release in the presence of PKC, Src and ERK inhibitors, whereas aspirin or p38 inhibitor had no effect on endostatin release. Despite VEGF or endostatin secretion, platelet releasates generated by stimulation with each galectin stimulated angiogenic responses in vitro including endothelial cell proliferation and tubulogenesis. The platelet angiogenic activity was independent of VEGF and was attributed to the concerted action of other proangiogenic molecules distinctly released by each galectin. Thus, secretion of platelet-derived angiogenic molecules may represent an alternative mechanism by which galectins promote angiogenic responses and its selective blockade may lead to the development of therapeutic strategies for angiogenesis-related diseases.
- Materia
-
Biotecnología de la Salud
Galectins
Platelet
VEGF - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
- OAI Identificador
- oai:digital.cic.gba.gob.ar:11746/7656
Ver los metadatos del registro completo
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spelling |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factorsEtulain, JuliaNegrotto, SoledadTribulatti, María VirginiaCroci, Diego OmarCarabelli, JulietaCampetella, Oscar EduardoRabinovich, Gabriel AdriánSchattner, Mirta AnaBiotecnología de la SaludGalectinsPlateletVEGFPlatelets contribute to vessel formation through the release of angiogenesis-modulating factors stored in their α-granules. Galectins, a family of lectins that bind β-galactoside residues, are up-regulated in inflammatory and cancerous tissues, trigger platelet activation and mediate vascularization processes. Here we aimed to elucidate whether the release of platelet-derived proangiogenic molecules could represent an alternative mechanism through which galectins promote neovascularization. We show that different members of the galectin family can selectively regulate the release of angiogenic molecules by human platelets. Whereas Galectin (Gal)-1, -3, and -8 triggered vascular endothelial growth factor (VEGF) release, only Gal-8 induced endostatin secretion. Release of VEGF induced by Gal-8 was partially prevented by COX-1, PKC, p38 and Src kinases inhibitors, whereas Gal-1-induced VEGF secretion was inhibited by PKC and ERK blockade, and Gal-3 triggered VEGF release selectively through a PKC-dependent pathway. Regarding endostatin, Gal-8 failed to stimulate its release in the presence of PKC, Src and ERK inhibitors, whereas aspirin or p38 inhibitor had no effect on endostatin release. Despite VEGF or endostatin secretion, platelet releasates generated by stimulation with each galectin stimulated angiogenic responses in vitro including endothelial cell proliferation and tubulogenesis. The platelet angiogenic activity was independent of VEGF and was attributed to the concerted action of other proangiogenic molecules distinctly released by each galectin. Thus, secretion of platelet-derived angiogenic molecules may represent an alternative mechanism by which galectins promote angiogenic responses and its selective blockade may lead to the development of therapeutic strategies for angiogenesis-related diseases.2014-04-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/7656spainfo:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0096402info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-09-04T09:43:38Zoai:digital.cic.gba.gob.ar:11746/7656Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-09-04 09:43:38.396CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse |
dc.title.none.fl_str_mv |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
title |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
spellingShingle |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors Etulain, Julia Biotecnología de la Salud Galectins Platelet VEGF |
title_short |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
title_full |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
title_fullStr |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
title_full_unstemmed |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
title_sort |
Control of angiogenesis by galectins involves the release of platelet-derived proangiogenic factors |
dc.creator.none.fl_str_mv |
Etulain, Julia Negrotto, Soledad Tribulatti, María Virginia Croci, Diego Omar Carabelli, Julieta Campetella, Oscar Eduardo Rabinovich, Gabriel Adrián Schattner, Mirta Ana |
author |
Etulain, Julia |
author_facet |
Etulain, Julia Negrotto, Soledad Tribulatti, María Virginia Croci, Diego Omar Carabelli, Julieta Campetella, Oscar Eduardo Rabinovich, Gabriel Adrián Schattner, Mirta Ana |
author_role |
author |
author2 |
Negrotto, Soledad Tribulatti, María Virginia Croci, Diego Omar Carabelli, Julieta Campetella, Oscar Eduardo Rabinovich, Gabriel Adrián Schattner, Mirta Ana |
author2_role |
author author author author author author author |
dc.subject.none.fl_str_mv |
Biotecnología de la Salud Galectins Platelet VEGF |
topic |
Biotecnología de la Salud Galectins Platelet VEGF |
dc.description.none.fl_txt_mv |
Platelets contribute to vessel formation through the release of angiogenesis-modulating factors stored in their α-granules. Galectins, a family of lectins that bind β-galactoside residues, are up-regulated in inflammatory and cancerous tissues, trigger platelet activation and mediate vascularization processes. Here we aimed to elucidate whether the release of platelet-derived proangiogenic molecules could represent an alternative mechanism through which galectins promote neovascularization. We show that different members of the galectin family can selectively regulate the release of angiogenic molecules by human platelets. Whereas Galectin (Gal)-1, -3, and -8 triggered vascular endothelial growth factor (VEGF) release, only Gal-8 induced endostatin secretion. Release of VEGF induced by Gal-8 was partially prevented by COX-1, PKC, p38 and Src kinases inhibitors, whereas Gal-1-induced VEGF secretion was inhibited by PKC and ERK blockade, and Gal-3 triggered VEGF release selectively through a PKC-dependent pathway. Regarding endostatin, Gal-8 failed to stimulate its release in the presence of PKC, Src and ERK inhibitors, whereas aspirin or p38 inhibitor had no effect on endostatin release. Despite VEGF or endostatin secretion, platelet releasates generated by stimulation with each galectin stimulated angiogenic responses in vitro including endothelial cell proliferation and tubulogenesis. The platelet angiogenic activity was independent of VEGF and was attributed to the concerted action of other proangiogenic molecules distinctly released by each galectin. Thus, secretion of platelet-derived angiogenic molecules may represent an alternative mechanism by which galectins promote angiogenic responses and its selective blockade may lead to the development of therapeutic strategies for angiogenesis-related diseases. |
description |
Platelets contribute to vessel formation through the release of angiogenesis-modulating factors stored in their α-granules. Galectins, a family of lectins that bind β-galactoside residues, are up-regulated in inflammatory and cancerous tissues, trigger platelet activation and mediate vascularization processes. Here we aimed to elucidate whether the release of platelet-derived proangiogenic molecules could represent an alternative mechanism through which galectins promote neovascularization. We show that different members of the galectin family can selectively regulate the release of angiogenic molecules by human platelets. Whereas Galectin (Gal)-1, -3, and -8 triggered vascular endothelial growth factor (VEGF) release, only Gal-8 induced endostatin secretion. Release of VEGF induced by Gal-8 was partially prevented by COX-1, PKC, p38 and Src kinases inhibitors, whereas Gal-1-induced VEGF secretion was inhibited by PKC and ERK blockade, and Gal-3 triggered VEGF release selectively through a PKC-dependent pathway. Regarding endostatin, Gal-8 failed to stimulate its release in the presence of PKC, Src and ERK inhibitors, whereas aspirin or p38 inhibitor had no effect on endostatin release. Despite VEGF or endostatin secretion, platelet releasates generated by stimulation with each galectin stimulated angiogenic responses in vitro including endothelial cell proliferation and tubulogenesis. The platelet angiogenic activity was independent of VEGF and was attributed to the concerted action of other proangiogenic molecules distinctly released by each galectin. Thus, secretion of platelet-derived angiogenic molecules may represent an alternative mechanism by which galectins promote angiogenic responses and its selective blockade may lead to the development of therapeutic strategies for angiogenesis-related diseases. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-04-07 |
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 |
https://digital.cic.gba.gob.ar/handle/11746/7656 |
url |
https://digital.cic.gba.gob.ar/handle/11746/7656 |
dc.language.none.fl_str_mv |
spa |
language |
spa |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0096402 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ |
dc.format.none.fl_str_mv |
application/pdf |
dc.source.none.fl_str_mv |
reponame:CIC Digital (CICBA) instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Aires instacron:CICBA |
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CIC Digital (CICBA) |
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CIC Digital (CICBA) |
instname_str |
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
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CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
repository.mail.fl_str_mv |
marisa.degiusti@sedici.unlp.edu.ar |
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12.623145 |