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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
来源:
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.
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页码:1069 / 1071
页数:3
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