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Opposite actions of urotensin II and relaxin‐2 on cellular expression of fibronectin in renal fibrosis: A preliminary experimental study
Author(s) -
Cernaro Valeria,
Medici Maria A,
Bianco Federica,
Santoro Domenico,
Lacquaniti Antonio,
Romeo Adolfo,
Lucisano Silvia,
Buemi Antoine,
Buemi Michele
Publication year - 2017
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12798
Subject(s) - urotensin ii , relaxin , fibronectin , medicine , endocrinology , western blot , fibrosis , receptor , chemistry , biology , microbiology and biotechnology , extracellular matrix , gene , biochemistry
Summary 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 ‐ PK 1 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.