Role of E-type prostaglandin receptor EP3 in the vasoconstrictor activity evoked by prostacyclin in thromboxane-prostanoid receptor deficient mice.
Role of E-type prostaglandin receptor EP3 in the vasoconstrictor activity evoked by prostacyclin in thromboxane-prostanoid receptor deficient mice.
复制标题
E型前列腺素受体EP3在血栓素-前列腺素受体缺陷小鼠中前列环素引起的血管收缩活性中的作用
DOI：
10.1038/srep42167
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发表时间：
2017-02-06
影响因子：
4.6
通讯作者：
Zhou Y
中科院分区：
文献类型：
--
作者：
Li Z;Zhang Y;Liu B;Luo W;Li H;Zhou Y
前列环素，也被称为前列腺素I2(PGI2)，在前列环素受体表达有限的情况下，引起血管收缩。尽管血栓素A-前列腺素受体(TP)被认为介导了PGI2的这种反应，但其他未知的受体(S)也可能参与其中。因此，设计了TP基因敲除(TP−/−)小鼠，并用来检验这一假设。通常对PGI2表现出收缩的血管被分离出来进行功能和生化分析。在此，我们发现，在TP−/−小鼠的腹主动脉中，PGI2引起的收缩反应确实只被部分消除。有趣的是，进一步拮抗E-型前列腺素受体EP3会去除剩余的收缩活动，导致PGI2在TP−/−小鼠的这类血管上引起的松弛。这些结果表明，EP3和TP共同参与了PGI2引起的血管收缩反应，从而暗示了内皮环氧合酶代谢产物(主要由PGI2组成)调节血管功能的新机制。
Prostacyclin, also termed as prostaglandin I2(PGI2), evokes contraction in vessels with limited expression of the prostacyclin receptor. Although the thromboxane-prostanoid receptor (TP) is proposed to mediate such a response of PGI2, other unknown receptor(s) might also be involved. TP knockout (TP−/−) mice were thus designed and used to test the hypothesis. Vessels, which normally show contraction to PGI2, were isolated for functional and biochemical analyses. Here, we showed that the contractile response evoked by PGI2was indeed only partially abolished in the abdominal aorta of TP−/−mice. Interestingly, further antagonizing the E-type prostaglandin receptor EP3 removed the remaining contractile activity, resulting in relaxation evoked by PGI2in such vessels of TP−/−mice. These results suggest that EP3 along with TP contributes to vasoconstrictor responses evoked by PGI2, and hence imply a novel mechanism for endothelial cyclooxygenase metabolites (which consist mainly of PGI2) in regulating vascular functions.