Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis

Autores
Ricci, Analía Gabriela; Olivares, Carla Noemi; Bilotas, Mariela Andrea; Meresman, Gabriela Fabiana; Barañao, Rosa Ines
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The main factor involved in neovascularization of ectopic endometrial tissue in endometriosis is the vascular endothelial growth factor (VEGF), which is produced both by the endometrial implant and by peritoneal macrophages. On the other hand, bevacizumab is an antiangiogenic agent used in the treatment of different tumors, like colorectal, pulmonary, and recently mammary. We evaluated the effect of the inhibition of VEGF activity with bevacizumab (Avastin) on ectopic endometrial growth in a murine model of endometriosis. Two months old female BALB/c mice had surgery performed to induce endometriotic-like lesions. Treatment with bevacizumab started on post-surgery day 15 and continued during 2 weeks. Then, animals were sacrificed, peritoneal fluid was collected, and endometriotic-like lesions were counted, measured, and removed. Cell proliferation, vascular density, and apoptosis were assessed by immunohistochemistry for proliferating cell nuclear antigen (PCNA), immunohistochemistry for CD34, and Terminal Deoxynucleotidil Transferase-Mediated dUTP Nick End Labeling (TUNEL), respectively. Vascular endothelial growth factor levels were evaluated in the peritoneal fluid by enzyme-linked immunoassay (ELISA). Treatment with bevacizumab significantly inhibited endometriotic lesion development (P <.05). Consistently, bevacizumab significantly inhibited cell proliferation in lesions (P <.01), reduced vascular density (P <.001), as well as increased the apoptotic cell percentage (P <.001). In addition, bevacizumab reduced VEGF levels in peritoneal fluid of endometriosis-induced animals (P <.05). In conclusion, this study suggests a direct effect of bevacizumab on the reduction of endometrial implant growth and supports further research on VEGF inhibition as a novel therapeutic modality in endometriosis. © The Author(s) 2011.
Fil: Ricci, Analía Gabriela. 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
Fil: Olivares, Carla Noemi. 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
Fil: Bilotas, Mariela Andrea. 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
Fil: Meresman, Gabriela Fabiana. 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
Fil: Barañao, Rosa Ines. 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
Materia
Apoptosis
Balb/C Mice
Bevacizumab
Cell Proliferation
Endometriosis
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/78704
Acceder
id CONICETDig_1f33804ca9b6d9dc06113c040beb5fc5
oai_identifier_str oai:ri.conicet.gov.ar:11336/78704
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosisRicci, Analía GabrielaOlivares, Carla NoemiBilotas, Mariela AndreaMeresman, Gabriela FabianaBarañao, Rosa InesApoptosisBalb/C MiceBevacizumabCell ProliferationEndometriosishttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The main factor involved in neovascularization of ectopic endometrial tissue in endometriosis is the vascular endothelial growth factor (VEGF), which is produced both by the endometrial implant and by peritoneal macrophages. On the other hand, bevacizumab is an antiangiogenic agent used in the treatment of different tumors, like colorectal, pulmonary, and recently mammary. We evaluated the effect of the inhibition of VEGF activity with bevacizumab (Avastin) on ectopic endometrial growth in a murine model of endometriosis. Two months old female BALB/c mice had surgery performed to induce endometriotic-like lesions. Treatment with bevacizumab started on post-surgery day 15 and continued during 2 weeks. Then, animals were sacrificed, peritoneal fluid was collected, and endometriotic-like lesions were counted, measured, and removed. Cell proliferation, vascular density, and apoptosis were assessed by immunohistochemistry for proliferating cell nuclear antigen (PCNA), immunohistochemistry for CD34, and Terminal Deoxynucleotidil Transferase-Mediated dUTP Nick End Labeling (TUNEL), respectively. Vascular endothelial growth factor levels were evaluated in the peritoneal fluid by enzyme-linked immunoassay (ELISA). Treatment with bevacizumab significantly inhibited endometriotic lesion development (P <.05). Consistently, bevacizumab significantly inhibited cell proliferation in lesions (P <.01), reduced vascular density (P <.001), as well as increased the apoptotic cell percentage (P <.001). In addition, bevacizumab reduced VEGF levels in peritoneal fluid of endometriosis-induced animals (P <.05). In conclusion, this study suggests a direct effect of bevacizumab on the reduction of endometrial implant growth and supports further research on VEGF inhibition as a novel therapeutic modality in endometriosis. © The Author(s) 2011.Fil: Ricci, Analía Gabriela. 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; ArgentinaFil: Olivares, Carla Noemi. 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; ArgentinaFil: Bilotas, Mariela Andrea. 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; ArgentinaFil: Meresman, Gabriela Fabiana. 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; ArgentinaFil: Barañao, Rosa Ines. 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; ArgentinaSAGE Publications2011-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/78704Ricci, Analía Gabriela; Olivares, Carla Noemi; Bilotas, Mariela Andrea; Meresman, Gabriela Fabiana; Barañao, Rosa Ines; Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis; SAGE Publications; Reproductive Sciences; 18; 7; 7-2011; 614-6221933-7191CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://journals.sagepub.com/doi/10.1177/1933719110395406info:eu-repo/semantics/altIdentifier/doi/10.1177/1933719110395406info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:24:08Zoai:ri.conicet.gov.ar:11336/78704instacron: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:34982025-09-10 13:24:08.734CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
title Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
spellingShingle Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
Ricci, Analía Gabriela
Apoptosis
Balb/C Mice
Bevacizumab
Cell Proliferation
Endometriosis
title_short Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
title_full Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
title_fullStr Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
title_full_unstemmed Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
title_sort Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis
dc.creator.none.fl_str_mv Ricci, Analía Gabriela
Olivares, Carla Noemi
Bilotas, Mariela Andrea
Meresman, Gabriela Fabiana
Barañao, Rosa Ines
author Ricci, Analía Gabriela
author_facet Ricci, Analía Gabriela
Olivares, Carla Noemi
Bilotas, Mariela Andrea
Meresman, Gabriela Fabiana
Barañao, Rosa Ines
author_role author
author2 Olivares, Carla Noemi
Bilotas, Mariela Andrea
Meresman, Gabriela Fabiana
Barañao, Rosa Ines
author2_role author
author
author
author
dc.subject.none.fl_str_mv Apoptosis
Balb/C Mice
Bevacizumab
Cell Proliferation
Endometriosis
topic Apoptosis
Balb/C Mice
Bevacizumab
Cell Proliferation
Endometriosis
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The main factor involved in neovascularization of ectopic endometrial tissue in endometriosis is the vascular endothelial growth factor (VEGF), which is produced both by the endometrial implant and by peritoneal macrophages. On the other hand, bevacizumab is an antiangiogenic agent used in the treatment of different tumors, like colorectal, pulmonary, and recently mammary. We evaluated the effect of the inhibition of VEGF activity with bevacizumab (Avastin) on ectopic endometrial growth in a murine model of endometriosis. Two months old female BALB/c mice had surgery performed to induce endometriotic-like lesions. Treatment with bevacizumab started on post-surgery day 15 and continued during 2 weeks. Then, animals were sacrificed, peritoneal fluid was collected, and endometriotic-like lesions were counted, measured, and removed. Cell proliferation, vascular density, and apoptosis were assessed by immunohistochemistry for proliferating cell nuclear antigen (PCNA), immunohistochemistry for CD34, and Terminal Deoxynucleotidil Transferase-Mediated dUTP Nick End Labeling (TUNEL), respectively. Vascular endothelial growth factor levels were evaluated in the peritoneal fluid by enzyme-linked immunoassay (ELISA). Treatment with bevacizumab significantly inhibited endometriotic lesion development (P <.05). Consistently, bevacizumab significantly inhibited cell proliferation in lesions (P <.01), reduced vascular density (P <.001), as well as increased the apoptotic cell percentage (P <.001). In addition, bevacizumab reduced VEGF levels in peritoneal fluid of endometriosis-induced animals (P <.05). In conclusion, this study suggests a direct effect of bevacizumab on the reduction of endometrial implant growth and supports further research on VEGF inhibition as a novel therapeutic modality in endometriosis. © The Author(s) 2011.
Fil: Ricci, Analía Gabriela. 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
Fil: Olivares, Carla Noemi. 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
Fil: Bilotas, Mariela Andrea. 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
Fil: Meresman, Gabriela Fabiana. 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
Fil: Barañao, Rosa Ines. 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
description The main factor involved in neovascularization of ectopic endometrial tissue in endometriosis is the vascular endothelial growth factor (VEGF), which is produced both by the endometrial implant and by peritoneal macrophages. On the other hand, bevacizumab is an antiangiogenic agent used in the treatment of different tumors, like colorectal, pulmonary, and recently mammary. We evaluated the effect of the inhibition of VEGF activity with bevacizumab (Avastin) on ectopic endometrial growth in a murine model of endometriosis. Two months old female BALB/c mice had surgery performed to induce endometriotic-like lesions. Treatment with bevacizumab started on post-surgery day 15 and continued during 2 weeks. Then, animals were sacrificed, peritoneal fluid was collected, and endometriotic-like lesions were counted, measured, and removed. Cell proliferation, vascular density, and apoptosis were assessed by immunohistochemistry for proliferating cell nuclear antigen (PCNA), immunohistochemistry for CD34, and Terminal Deoxynucleotidil Transferase-Mediated dUTP Nick End Labeling (TUNEL), respectively. Vascular endothelial growth factor levels were evaluated in the peritoneal fluid by enzyme-linked immunoassay (ELISA). Treatment with bevacizumab significantly inhibited endometriotic lesion development (P <.05). Consistently, bevacizumab significantly inhibited cell proliferation in lesions (P <.01), reduced vascular density (P <.001), as well as increased the apoptotic cell percentage (P <.001). In addition, bevacizumab reduced VEGF levels in peritoneal fluid of endometriosis-induced animals (P <.05). In conclusion, this study suggests a direct effect of bevacizumab on the reduction of endometrial implant growth and supports further research on VEGF inhibition as a novel therapeutic modality in endometriosis. © The Author(s) 2011.
publishDate 2011
dc.date.none.fl_str_mv 2011-07
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 http://hdl.handle.net/11336/78704
Ricci, Analía Gabriela; Olivares, Carla Noemi; Bilotas, Mariela Andrea; Meresman, Gabriela Fabiana; Barañao, Rosa Ines; Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis; SAGE Publications; Reproductive Sciences; 18; 7; 7-2011; 614-622
1933-7191
CONICET Digital
CONICET
url http://hdl.handle.net/11336/78704
identifier_str_mv Ricci, Analía Gabriela; Olivares, Carla Noemi; Bilotas, Mariela Andrea; Meresman, Gabriela Fabiana; Barañao, Rosa Ines; Effect of vascular endothelial growth factor inhibition on endometrial implant development in a murine model of endometriosis; SAGE Publications; Reproductive Sciences; 18; 7; 7-2011; 614-622
1933-7191
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://journals.sagepub.com/doi/10.1177/1933719110395406
info:eu-repo/semantics/altIdentifier/doi/10.1177/1933719110395406
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv SAGE Publications
publisher.none.fl_str_mv SAGE Publications
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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