Please use this identifier to cite or link to this item:
https://hdl.handle.net/20.500.12530/21559
Title: | TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2. | |
Authors: | ||
Mesh: | ||
Issue Date: | 2015 | |
Citation: | Mediators Inflamm..2015;(2015):506041 | |
Abstract: | 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-β is considered the main fibrogenic cytokine; however, in some pathological settings TGF-β also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-β, but data on TGF-β role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF-β 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-β blockade, using an anti-TGF-β 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-β 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-β exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic target. | |
PMID: | 26074680 | |
URI: | https://hdl.handle.net/20.500.12530/21559 | |
Rights: | openAccess | |
Appears in Collections: | Fundaciones e Institutos de Investigación > IIS H. U. La Paz > Artículos | |
Files in This Item:
File | Description | Size | Format | |
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PMC4436472.pdf | 1.96 MB | Adobe PDF | View/Open |
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