Urotensin II is an autocrine/paracrine growth factor for aortic adventitia of rat

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• 作者：Yonggang Zhang ; Yuguang Li ; Ruihong Wei ; Zhijian Wang ; Dingfang Bu ; Jing Zhao ; Yongzheng Pang ; Chaoshu Tang
• 关键词：Adventitial fibroblasts ; Peptide ; GPR₁₄ ; Receptor ; Collagen ; Vascular remodeling ; Proliferation
• 刊名：Regulatory Peptides
• 出版年：2008
• 出版时间：29 November 2008
• 年：2008
• 卷：151
• 期：1-3
• 页码：88-94
• 全文大小：1624 K

文摘

Urotensin II (UII) is a potent vasoconstrictive peptide; however, its significance in vascular adventitia has not been clearly elucidated. In this study, rat aortic adventitia showed mRNA expression and immunoreactivity of UII and its receptor (UT). Moreover, radioligand-binding assay showed that maximum binding capacity (Bmax) of [¹²⁵I]-UII was higher in adventitia than in media (28.60 ± 1.94 vs. 20.21 ± 1.11 fmol/mg, P < 0.01), with no difference in binding affinity (dissociation constant [Kd] 4.27 ± 0.49 vs. 4.60 ± 0.40 nM, P > 0.05). Furthermore, in cultured adventitial fibroblasts, UII stimulated DNA synthesis, collagen synthesis and secretion in a concentration-dependent manner. These effects were inhibited by the UII receptor antagonist urantide (10^− 6 mol/l), Ca²⁺ channel blocker nicardipine (10^− 5 mol/l), protein kinase C inhibitor H7 (10^− 6 mol/l), and mitogen-activated protein kinase inhibitor PD98059 (10^− 6 mol/l) but not the phosphatidyl inositol-3 kinase inhibitor wortmannin (10^− 7 mol/l). UII may act as an autocrine/paracrine factor through its receptor and the Ca²⁺ channel, protein kinase C, and mitogen-activated protein kinase signal transduction pathways, in the pathogenesis of vascular remodeling by activating vascular adventitia.