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16 December 2016 : Animal Research  

Substance P Inhibits the Collagen Synthesis of Rat Myocardial Fibroblasts Induced by Ang II

Zhiyong Yang1ABCDEF*, Xinzhong Zhang1ABCDE, Naipeng Guo1ABCD, Bin Li1BCD, Sheng Zhao2CD

DOI: 10.12659/MSM.898454

Med Sci Monit 2016; 22:4937-4946

Abstract

BACKGROUND: The aim of this study was to explore the regulating effects of Substance P (SP) on the collagen synthesis of rat myocardial fibroblasts (CFBs) induced by angiotensin II (Ang II) and its potential mechanism.

MATERIAL AND METHODS: The CFBs of a neonatal SD rat were separately cultured and divided into the control group, Ang II treatment group, and treatment groups with different concentrations of SP, Ang II +; each group was given corresponding treatment respectively.

RESULTS: Ang II successfully induced the collagen synthesis of CFBs. Compared with the control group, the phosphorylation levels of TGF-β, erk, and smad2/3 were higher (p<0.05). Different concentrations of SP had an effect on Ang II-induced CFBs, reduced the collagen synthesis of CFBs, and increased the expressions of SP receptors, accompanied by lowering TGF-β protein, erk protein phosphorylation level, and smad2/3 protein phosphorylation level (p<0.05). Moreover, the higher the concentrations of SP, the more obvious of an effect it exerted. Treating the Ang II + SP group with aprepitant reduced the inhibiting effects of SP on collagen synthesis. The expression changes of collagen I and collagen III detected by immunocytochemistry were exactly in accordance with the results of qPCR and Western blotting.

CONCLUSIONS: SP can inhibit collagen synthesis of CFBs after Ang II inducing which may adjust the downstream signaling pathways associated protein including TGF-β, erk and smad2/3. SP can block the progress of myocardial fibrosis and is dose dependent, which is expected to be a promising target for the treatment of myocardial fibrosis.

Keywords: Angiotensin II - pharmacology, Cells, Cultured, Collagen - biosynthesis, Collagen Type I - metabolism, Collagen Type III - metabolism, Fibroblasts - metabolism, Fibrosis, Heart - drug effects, Myocardium - pathology, Rats, Rats, Sprague-Dawley, Signal Transduction - drug effects, Smad2 Protein - metabolism, Smad3 Protein - metabolism, Substance P - pharmacology, Transforming Growth Factor beta

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750