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...
| Autores: | , , , , , , , |
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| 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 |
| Sumario: | 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 |
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