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
CIC Digital (CICBA)
Institución
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
OAI Identificador
oai:digital.cic.gba.gob.ar:11746/7656

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network_acronym_str CICBA
repository_id_str 9441
network_name_str CIC Digital (CICBA)
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
reponame_str CIC Digital (CICBA)
collection CIC Digital (CICBA)
instname_str Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
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institution CICBA
repository.name.fl_str_mv 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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