Alteration of vascular urotensin II receptor in mice with apolipoprotein E gene knockout

Urotensin II (U-II), originally identified as a fish neuropeptide, exerts a broad spectrum of biological functions and is considered to be the most potent vasoconstrictor in mammals. Recently the intense staining of U-II-like immunoreactivity within coronary atheroma and the effect of mitogenic in v...

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Published inPeptides (New York, N.Y. : 1980) Vol. 27; no. 4; pp. 858 - 863
Main Authors Wang, Zhi Jian, Shi, Li Bin, Xiong, Zhuo Wei, Zhang, Li Fang, Meng, Lei, Bu, Ding Fang, Tang, Chao Shu, Ding, Wen Hui
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.04.2006
Elsevier Science
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Summary:Urotensin II (U-II), originally identified as a fish neuropeptide, exerts a broad spectrum of biological functions and is considered to be the most potent vasoconstrictor in mammals. Recently the intense staining of U-II-like immunoreactivity within coronary atheroma and the effect of mitogenic in vascular smooth muscle cells (VSMCs) suggest that U-II is possibly a proatherogenic factor in the pathogenesis of cardiovascular diseases (CVD). In the present study, we analyzed the gene expression of U-II and GPR14, a high-affinity receptor for U-II, in aorta of apolipoprotein E (apoE) −/− mutant mice by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Compared with wild-type mice at the same age group, GPR14 mRNA level is significant increase in aorta of apoE −/− mice at age of 18, 28 and 38 weeks, respectively. The increased GPR14 mRNA level was 54.2, 50.0 and 97.0% in the three age groups, respectively. We did not detect U-II mRNA expression in aorta either in apoE −/− mice or in wild-type mice. In 28-week mice, ligand-binding assay showed that maximum binding capacity ( B max) of 125I-U-II aorta from apoE −/− mice was increased by 64%, while the affinity of the binding did not change compared with that of wild-type mice. These results indicate that the up-regulation of vascular U-II receptor (UT), GPR14 might be involved in the pathogenesis of atherosclerosis.
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ISSN:0196-9781
1873-5169
DOI:10.1016/j.peptides.2005.08.028