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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。
Objective To observe the change of urotensin Ⅱ receptor-GPR14 expression in aortic tissue of apoE knockout mice in order to investigate the role of UⅡ and its receptor system in the pathogenesis of atherosclerosis. Methods C57BL / 6J mice (n = 6 in each subgroup) of apoE gene knockout and age-matched control (18, 28 and 38 weeks) were obtained. Results The GPR14 expression in apoE knockout mice increased 54.2% (18 weeks, P <0.05), 50.0% (28 weeks, P <0.05) and 97.0% (38 weeks, P <0.01) compared with the controls. The apoE gene knockout and age-matched control mice (n = 8) were given a radioactive isotope of 125I-urotensin II and the maximal binding capacity (apoE) of the apoE gene knockout group was increased 64% (P <0.01), while Kd value of dissociation constant had no significant change (P> 0.05). Conclusion Urotensin Ⅱ / GPR14 pathway may be involved in the pathogenesis of atherosclerosis.