Yun Mi-Ran, Okajima Fumikazu, Im Dong-Soon
Laboratory of Pharmacology, College of Pharmacy, Pusan National University, Busan, Republic of Korea.
J Pharmacol Sci. 2004 Jan;94(1):45-50. doi: 10.1254/jphs.94.45.
To elucidate the action and signal transduction of lysophosphatidylcholine (LPC), we challenged a set of LPC on U937 human monocytes and found that LPC mobilized Ca(2+). The Ca(2+) response was not blocked by pertussis toxin, an inhibitor of G(i/o) proteins, or by U73122, a phospholipase C inhibitor. Furthermore, the response was totally blocked by addition of EGTA to the extracellular media, suggesting that Ca(2+) influx across the plasma membrane was the only source of LPC-induced Ca(2+) response in the U937 cells. 16:0 and 18:0 LPC induced similar responses. Recently it has been suggested that two G protein-coupled receptors function as LPC receptors in the plasma membrane. RT-PCR analysis indicated that neither the G2A receptor nor the GPR4 receptor is expressed in the U937 monocytes. Our data suggests that another action mechanism of LPC may be involved in the LPC response in the U937 cells.
为阐明溶血磷脂酰胆碱(LPC)的作用及信号转导,我们用一系列LPC刺激U937人单核细胞,发现LPC可动员Ca(2+)。百日咳毒素(一种G(i/o)蛋白抑制剂)或U73122(一种磷脂酶C抑制剂)均不能阻断Ca(2+)反应。此外,向细胞外培养基中添加EGTA可完全阻断该反应,这表明跨质膜的Ca(2+)内流是U937细胞中LPC诱导的Ca(2+)反应的唯一来源。16:0和18:0 LPC诱导的反应相似。最近有研究表明,两种G蛋白偶联受体在质膜中作为LPC受体发挥作用。逆转录-聚合酶链反应(RT-PCR)分析表明,U937单核细胞中既不表达G2A受体也不表达GPR4受体。我们的数据表明,LPC的另一种作用机制可能参与了U937细胞中的LPC反应。