Our aim was to evaluate the role of urotensin II, urantide (urotensin II receptor antagonist) and relaxin-2 on the cellular expression of fibronectin as a surrogate marker for renal fibrosis. We employed LLC-PK1 renal tubular epithelial cells and assessed the influence on the fibrotic process of the above-mentioned substances by using anti-fibronectin antibodies in western blot analysis. The addition of urotensin II increased fibronectin expression. Urantide reduced the positivity for fibronectin caused by urotensin II (P<.05). The anti-fibrotic action was more evident for relaxin-2 (P<.01). Also in the model of TGF-β1-induced fibrosis, urantide and, to a greater extent, relaxin-2 were able to significantly lessen fibronectin expression (respectively, P<.05 and P<.01). In conclusion, relaxin-2 may reduce urotensin II-induced renal fibrosis.
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