Opposite actions of urotensin II and relaxin-2 on cellular expression of fibronectin in renal fibrosis: A preliminary experimental study

被引:3
|
作者
Cernaro, Valeria [1 ]
Medici, Maria A. [2 ]
Bianco, Federica [2 ]
Santoro, Domenico [1 ]
Lacquaniti, Antonio [1 ]
Romeo, Adolfo [1 ]
Lucisano, Silvia [1 ]
Buemi, Antoine [1 ]
Buemi, Michele [1 ]
机构
[1] Univ Messina, Chair Nephrol, Dept Clin & Expt Med Univ, Via Consolare Valeria 1, I-98124 Messina, Italy
[2] Univ Messina, Dept Biol & Environm Sci, Messina, Italy
关键词
fibronectin; fibrosis; relaxin-2; urantide; urotensin II; NEONATAL CARDIAC FIBROBLASTS; INDUCED COLLAGEN-SYNTHESIS; TUBULOINTERSTITIAL FIBROSIS; IN-VIVO; PROGRESSION; FAILURE; HYPERTENSION; INVOLVEMENT; DYSFUNCTION; DISEASE;
D O I
10.1111/1440-1681.12798
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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-1-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.
引用
收藏
页码:1069 / 1071
页数:3
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