Urotensin II promotes monocyte chemoattractant protein-1 expression in aortic adventitial fibroblasts of rat.

Yonggang Zhang; Shilin Bao; Zejian Kuang; Yanjun MA; Yanchao HU; Yanyan Mao

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Urotensin II promotes monocyte chemoattractant protein-1 expression in aortic adventitial fibroblasts of rat.

Author: Yonggang ZHANG ^{1
,

2} ; Shilin BAO ³ ; Zejian KUANG ⁴ ; Yanjun MA ³ ; Yanchao HU ³ ; Yanyan MAO ³
Author Information

1. Department of Cardiology, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong 515041, China
2. Cardiovascular Laboratory, Centre for Translational Medicine, Shantou University Medical College, Shantou, Guangdong 515041, China. Email: zhangyg8686@hotmail.com.
3. Department of Cardiovascular Diseases, First Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong 515041, China.
4. Department of Cardiology, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong 515041, China.
Publication Type:Journal Article
MeSH: Adventitia; cytology; Animals; Aorta; cytology; Cells, Cultured; Chemokine CCL2; genetics; metabolism; Fibroblasts; drug effects; metabolism; Male; RNA, Messenger; genetics; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; Urotensins; pharmacology
From: Chinese Medical Journal 2014;127(10):1907-1912
CountryChina
Language:English
Abstract:
BACKGROUNDUrotensin II (UII), a potent vasoconstrictive peptide, is able to stimulate phenotypic differentiation of adventitial fibroblasts. This study aimed to determine the effect of UII on monocyte chemoattractant protein-1 (MCP-1) expression in rat aortic adventitial fibroblasts, so as to explore possible mechanisms in the development of vascular inflammation.
METHODSGrowth-arrested adventitial fibroblasts were incubated in serum-free medium with UII (10(-10)-10(-7) mol/L) and inhibitors of signal transduction pathways for 1 to 24 hours. MCP-1 mRNA and protein expression and secretion were determined by RT-PCR, Western blotting analysis and enzyme-linked immunosorbent assay (ELISA), respectively.
RESULTSUII dose- and time-dependently promoted MCP-1 mRNA and protein expression and secretion in cells, with maximal effect at 10(-8) mol/L at 3 hours for mRNA expression, 24 hours for protein expression in the cells, and 12 hours for protein secretion from the cells. Furthermore, the UII effects were significantly inhibited by treatment with its receptor antagonist SB710411, Rho kinase inhibitor Y27632, protein kinase C (PKC) inhibitor H7, mitogen-activated protein kinase inhibitor PD98059, calcineurin inhibitor cyclosporine A, and the Ca(2+)channel blocker nicardipine.
CONCLUSIONUII may stimulate MCP-1 expression in rat aortic adventitial fibroblasts through its receptor and Rho kinase, PKC, mitogen-activated protein kinase, calcineurin and Ca(2+) channel signal transduction, thus contributing to adventitial inflammation.