摘要
目的观察apoE敲除小鼠主动脉组织尾加压素Ⅱ受体-GPR14表达的变化,以探讨UⅡ及其受体系统在动脉粥样硬化发病中的作用。方法取不同周龄(18、28和38周)的apoE基因敲除及同龄对照C57BL/6J小鼠(各亚组n=6只),取主动脉,提取mRNA,行竞争RT-PCR。结果apoE敲除小鼠GPR14表达分别较同龄对照增加54.2%(18周,P<0.05)、50.0%(28周,P<0.05)、97.0%(38周,P<0.01)。取28周apoE基因敲除及同龄对照小鼠(各8只)主动脉行[125I]-尾加压素Ⅱ放射性配基实验,apoE基因敲除组最大结合力(Bmax)较对照组增大64%(P<0.01),而解离常数Kd值无明显变化(P>0.05)。结论尾加压素Ⅱ/GPR14通路可能参与动脉粥样硬化的发病过程。
AIM: To investigate the expression of the urotensin Ⅱ (UⅡ ) receptor GPR14 in the aorta of apoE knockout mouse. METHODS: The expression of GPR14 in the aorta of apoE knockout C57BL/6J mice at various ages ( 18 weeks, 28 weeks, and 38 weeks old, respectively) was determined with competitive RT- PCR. A binding assay of [^125I] - UⅡ on the aortic tissue was also performed in 28 weeks group. RESULTS: We found significant upregulation of GPR14 mRNA at all three ages. Compared with wild type group at the same age, the GPR14 mRNA level in apoE knockout mice increased 54.2% in 18 week group ( P 〈 0.05), 50.0% in 28 weeks group ( P 〈 0.05) and 97.0% in 38 weeks group ( P 〈 0.01). In the knockout group or in the wild type group, expressions of GPR14 in the 28 weeks time point were significantly higher than that in other two age groups, and there was no difference between the 18 weeks and 38 weeks group. In the binding assay, the Bmax of [^125I] - UⅡ to the aorta of apoE knockout mouse at 28 weeks increased 64% compared with the wild type ( P 〈 0.01 ), and no difference about the Kd between the two groups was observed. CONCLUSION: UⅡ and its receptor probably play an important role in the development of atherosclerosis.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第11期2081-2085,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.30270541)