TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2.

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.

journal_name

Mediators Inflamm

authors

Rodrigues-Díez R,Rayego-Mateos S,Orejudo M,Aroeira LS,Selgas R,Ortiz A,Egido J,Ruiz-Ortega M

doi

10.1155/2015/506041

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

506041

eissn

0962-9351

issn

1466-1861

journal_volume

2015

pub_type

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