Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells
- Autores
- Manzi, Malena; Bacigalupo, Maria Lorena; Carabias, Pablo; Elola, Maria Teresa; Wolfenstein, Carlota Elisa; Rabinovich, Gabriel Adrián; Espelt, Maria Victoria; Troncoso, María Fernanda
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Galectin-1 (Gal1), a beta-galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness and metastasis. During the early stages of HCC, transforming growth factor beta1 (TGF-B1 ) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-B1 and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-B1 in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-B1 induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-B1 -induced growth inhibition. Our results suggest that Gal1 and TGF-B1 might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis and angiogenesis
Fil: Manzi, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Bacigalupo, Maria Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Carabias, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Elola, Maria Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Wolfenstein, Carlota Elisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Espelt, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Troncoso, María Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina - Materia
-
Galectin-1
Hepatocellular Carcinoma Microenvironment
Sk-Hep-1 Cells
Sinusoidal Endothelial Cells
Transforming Growth Factor Beta1 - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/24025
Ver los metadatos del registro completo
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Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cellsManzi, MalenaBacigalupo, Maria LorenaCarabias, PabloElola, Maria TeresaWolfenstein, Carlota ElisaRabinovich, Gabriel AdriánEspelt, Maria VictoriaTroncoso, María FernandaGalectin-1Hepatocellular Carcinoma MicroenvironmentSk-Hep-1 CellsSinusoidal Endothelial CellsTransforming Growth Factor Beta1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Galectin-1 (Gal1), a beta-galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness and metastasis. During the early stages of HCC, transforming growth factor beta1 (TGF-B1 ) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-B1 and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-B1 in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-B1 induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-B1 -induced growth inhibition. Our results suggest that Gal1 and TGF-B1 might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis and angiogenesisFil: Manzi, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Bacigalupo, Maria Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Carabias, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Elola, Maria Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Wolfenstein, Carlota Elisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Espelt, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Troncoso, María Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaWiley2016-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/24025Manzi, Malena; Bacigalupo, Maria Lorena; Carabias, Pablo; Elola, Maria Teresa; Wolfenstein, Carlota Elisa; et al.; Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells; Wiley; Journal of Cellular Physiology; 231; 7; 7-2016; 1522-15330021-95411097-4652CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/jcp.25244/abstractinfo:eu-repo/semantics/altIdentifier/doi/10.1002/jcp.25244info:eu-repo/semantics/altIdentifier/url/26551914info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:20:03Zoai:ri.conicet.gov.ar:11336/24025instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:20:03.859CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| title |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| spellingShingle |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells Manzi, Malena Galectin-1 Hepatocellular Carcinoma Microenvironment Sk-Hep-1 Cells Sinusoidal Endothelial Cells Transforming Growth Factor Beta1 |
| title_short |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| title_full |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| title_fullStr |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| title_full_unstemmed |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| title_sort |
Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells |
| dc.creator.none.fl_str_mv |
Manzi, Malena Bacigalupo, Maria Lorena Carabias, Pablo Elola, Maria Teresa Wolfenstein, Carlota Elisa Rabinovich, Gabriel Adrián Espelt, Maria Victoria Troncoso, María Fernanda |
| author |
Manzi, Malena |
| author_facet |
Manzi, Malena Bacigalupo, Maria Lorena Carabias, Pablo Elola, Maria Teresa Wolfenstein, Carlota Elisa Rabinovich, Gabriel Adrián Espelt, Maria Victoria Troncoso, María Fernanda |
| author_role |
author |
| author2 |
Bacigalupo, Maria Lorena Carabias, Pablo Elola, Maria Teresa Wolfenstein, Carlota Elisa Rabinovich, Gabriel Adrián Espelt, Maria Victoria Troncoso, María Fernanda |
| author2_role |
author author author author author author author |
| dc.subject.none.fl_str_mv |
Galectin-1 Hepatocellular Carcinoma Microenvironment Sk-Hep-1 Cells Sinusoidal Endothelial Cells Transforming Growth Factor Beta1 |
| topic |
Galectin-1 Hepatocellular Carcinoma Microenvironment Sk-Hep-1 Cells Sinusoidal Endothelial Cells Transforming Growth Factor Beta1 |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
Galectin-1 (Gal1), a beta-galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness and metastasis. During the early stages of HCC, transforming growth factor beta1 (TGF-B1 ) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-B1 and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-B1 in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-B1 induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-B1 -induced growth inhibition. Our results suggest that Gal1 and TGF-B1 might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis and angiogenesis Fil: Manzi, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Bacigalupo, Maria Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Carabias, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Elola, Maria Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Wolfenstein, Carlota Elisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina Fil: Espelt, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Troncoso, María Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina |
| description |
Galectin-1 (Gal1), a beta-galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness and metastasis. During the early stages of HCC, transforming growth factor beta1 (TGF-B1 ) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-B1 and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-B1 in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-B1 induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-B1 -induced growth inhibition. Our results suggest that Gal1 and TGF-B1 might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis and angiogenesis |
| publishDate |
2016 |
| dc.date.none.fl_str_mv |
2016-07 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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http://hdl.handle.net/11336/24025 Manzi, Malena; Bacigalupo, Maria Lorena; Carabias, Pablo; Elola, Maria Teresa; Wolfenstein, Carlota Elisa; et al.; Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells; Wiley; Journal of Cellular Physiology; 231; 7; 7-2016; 1522-1533 0021-9541 1097-4652 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/24025 |
| identifier_str_mv |
Manzi, Malena; Bacigalupo, Maria Lorena; Carabias, Pablo; Elola, Maria Teresa; Wolfenstein, Carlota Elisa; et al.; Galectin-1 controls the proliferation and migration of liver Sinusoidal endothelial cells and their interaction with hepatocarcinoma cells; Wiley; Journal of Cellular Physiology; 231; 7; 7-2016; 1522-1533 0021-9541 1097-4652 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/jcp.25244/abstract info:eu-repo/semantics/altIdentifier/doi/10.1002/jcp.25244 info:eu-repo/semantics/altIdentifier/url/26551914 |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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openAccess |
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