New function of LPA3 receptor that regulates vagal afferent nerves activation

在本研究中，我们评估了LPA3信号诱导迷走神经兴奋和定量LPA和其他溶血磷脂水平在心肌梗死中的作用。我们发现，在急性缺血损伤模型中，注射LPA3激动剂T13(类似于2-酰基LPA)显著减少实际面积。我们用LC-MS/MS分析了急性冠脉综合征(ACS)患者的临床标本(血浆)，发现不饱和LPA选择性地升高了对LPA3具有强烈激动剂活性。此外，其他不饱和溶血磷脂(LPC、LPE、LPG、LPI、LysoPS)也有所增加。这些结果表明，不饱和LPA是由于心肌梗死时自体趋化蛋白底物增加而产生的。

In this study, we assessed the functional effects of LPA3 signal-induced vagal excitation and quantifying LPA and other lysophospholipids level in myocardial infarction.We found that injection of LPA3 agonist named T13, which is 2-acyl LPA analog, significantly decreased infact area in acute ischemic injury model. We analyzed clinical specimen (plasma) from acute coronary syndrome (ACS) patients by LC-MS/MS, and found unsaturated LPA, which show potent agonist activity for LPA3, were selectively elevated in ACS. In addition, other unsaturated lysophospholipids (LPC, LPE, LPG, LPI, LysoPS) were also increased. These results suggest that unsaturated LPA are produced by increased substrates of autotaxin in myocardial infarction.