Urotensin II promotes monocyte chemoattractant protein-1 expression in aortic adventitial fibroblasts of rat / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 1907-1912, 2014.
Article
Dans Anglais
| WPRIM
| ID: wpr-248082
ABSTRACT
<p><b>BACKGROUND</b>Urotensin 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.</p><p><b>METHODS</b>Growth-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.</p><p><b>RESULTS</b>UII 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.</p><p><b>CONCLUSION</b>UII 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.</p>
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Aorte
/
Pharmacologie
/
Urotensines
/
ARN messager
/
Cellules cultivées
/
Rat Sprague-Dawley
/
Chimiokine CCL2
/
RT-PCR
/
Biologie cellulaire
/
Fibroblastes
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Chinese Medical Journal
Année:
2014
Type:
Article
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