TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2

The CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF- is considered the main fibrogenic cytokine; however, in some patho...

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Autores: Rodrigues Díez, Raquel, Rayego-Mateos, Sandra, Orejudo, Macarena, Aroeira, Luiz Stark, Selgas, Rafael, Ortiz Arduán, Alberto, Egido de los Ríos, Jesús, Ruiz Ortega, Marta
Tipo de recurso: artículo
Fecha de publicación:2015
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/672362
Acceso en línea:http://hdl.handle.net/10486/672362
https://dx.doi.org/10.1155/2015/506041
Access Level:acceso abierto
Palabra clave:Tissue growth factor
Renal disease
CCN2
TGF-
Medicina
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spelling TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2Rodrigues Díez, RaquelRayego-Mateos, SandraOrejudo, MacarenaAroeira, Luiz StarkSelgas, RafaelOrtiz Arduán, AlbertoEgido de los Ríos, JesúsRuiz Ortega, MartaTissue growth factorRenal diseaseCCN2TGF-MedicinaThe CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF- is considered the main fibrogenic cytokine; however, in some pathological settings TGF- also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-, but data on TGF- role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF- blockade in CCN2-mediated experimental renal damage. Systemic administration of the C-terminal module of CCN2 to mice caused sustained renal inflammation. In these mice, TGF- blockade, using an anti-TGF- neutralizing antibody, significantly increased renal expression of the NGAL (a kidney injury biomarker), kidney infiltration by monocytes/macrophages, and upregulation of MCP-1 expression. The anti-inflammatory effect of TGF- seems to be mediated by a dysregulation of the systemic Treg immune response, shown by decreased levels of circulating CD4+/Foxp3+Treg cells. Our experimental data support the idea that TGF- exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic targetThis work was supported by grants from Impulsion grant of the ERA-EDTA Working Group on Immunonephrology, the Instituto de Salud Carlos III (ISCIII-RETIC RD12/0021 Fondos FEDER REDINREN, PI081564, PI11/01854, PI13/00047, and PI14/00041), FRIATIRSIN, Comunidad de Madrid (Fibroteam S2010/BMD- 2321, CIFRA S2010/BMD-2378), Sociedad Española de Nefrología, FP7-HEALTH-2013-INNOVATION-1-602422, and Programa Intensificación Actividad Investigadora (ISCIII/Agencia Laín-Entralgo/CM) to Alberto Ortiz. Raquel Rodrigues-Díez is a fellow of ERA-EDTA.Hindawi Publishing CorporationDepartamento de MedicinaFacultad de MedicinaInstituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)Instituto de Investigación Sanitaria del Hospital Universitario de La Paz (IdiPAZ)20152015-01-01research articlehttp://purl.org/coar/resource_type/c_2df8fbb1VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10486/672362https://dx.doi.org/10.1155/2015/506041reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.uam.es:10486/6723622026-06-23T12:46:27Z
dc.title.none.fl_str_mv TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
title TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
spellingShingle TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
Rodrigues Díez, Raquel
Tissue growth factor
Renal disease
CCN2
TGF-
Medicina
title_short TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
title_full TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
title_fullStr TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
title_full_unstemmed TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
title_sort TGF-beta blockade increases renal inflammation caused by the C-terminal module of the CCN2
dc.creator.none.fl_str_mv Rodrigues Díez, Raquel
Rayego-Mateos, Sandra
Orejudo, Macarena
Aroeira, Luiz Stark
Selgas, Rafael
Ortiz Arduán, Alberto
Egido de los Ríos, Jesús
Ruiz Ortega, Marta
author Rodrigues Díez, Raquel
author_facet Rodrigues Díez, Raquel
Rayego-Mateos, Sandra
Orejudo, Macarena
Aroeira, Luiz Stark
Selgas, Rafael
Ortiz Arduán, Alberto
Egido de los Ríos, Jesús
Ruiz Ortega, Marta
author_role author
author2 Rayego-Mateos, Sandra
Orejudo, Macarena
Aroeira, Luiz Stark
Selgas, Rafael
Ortiz Arduán, Alberto
Egido de los Ríos, Jesús
Ruiz Ortega, Marta
author2_role author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Departamento de Medicina
Facultad de Medicina
Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)
Instituto de Investigación Sanitaria del Hospital Universitario de La Paz (IdiPAZ)
dc.subject.none.fl_str_mv Tissue growth factor
Renal disease
CCN2
TGF-
Medicina
topic Tissue growth factor
Renal disease
CCN2
TGF-
Medicina
description The CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF- is considered the main fibrogenic cytokine; however, in some pathological settings TGF- also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-, but data on TGF- role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF- blockade in CCN2-mediated experimental renal damage. Systemic administration of the C-terminal module of CCN2 to mice caused sustained renal inflammation. In these mice, TGF- blockade, using an anti-TGF- neutralizing antibody, significantly increased renal expression of the NGAL (a kidney injury biomarker), kidney infiltration by monocytes/macrophages, and upregulation of MCP-1 expression. The anti-inflammatory effect of TGF- seems to be mediated by a dysregulation of the systemic Treg immune response, shown by decreased levels of circulating CD4+/Foxp3+Treg cells. Our experimental data support the idea that TGF- exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic target
publishDate 2015
dc.date.none.fl_str_mv 2015
2015-01-01
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10486/672362
https://dx.doi.org/10.1155/2015/506041
url http://hdl.handle.net/10486/672362
https://dx.doi.org/10.1155/2015/506041
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hindawi Publishing Corporation
publisher.none.fl_str_mv Hindawi Publishing Corporation
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301603

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