Park Kyoung Sun, Lee Ha Young, Kim Mi-Kyoung, Shin Eun Ha, Bae Yoe-Sik
Medical Research Center for Cancer Molecular Therapy, College of Medicine, Dong-A University, Busan 602-714, Republic of Korea.
Biochem Biophys Res Commun. 2005 Jul 29;333(2):353-8. doi: 10.1016/j.bbrc.2005.05.109.
In this study, we observed that lysophosphatidylserine (LPS) stimulated intracellular calcium (Ca(2+)) increase in leukemic cells but not in normal human peripheral blood mononuclear cells. LPS also stimulated Ca(2+) increase in human leukemic THP-1 cells. LPS-stimulated Ca(2+) increase was inhibited by U-73122 but not by U-73343. LPS also stimulated inositol phosphates formation in THP-1 cells, suggesting that LPS stimulates calcium signaling via phospholipase C activation. Moreover, pertussis toxin (PTX) completely inhibited Ca(2+) increase by LPS, indicating the activation of PTX-sensitive G-proteins. We also found that LPS-induced Ca(2+) increase was completely inhibited by suramin, suggesting G-protein coupled receptor activation. Since LPS specifically stimulates PTX-sensitive G-proteins, phospholipase C-dependent Ca(2+) increase in leukemic cells but not normal peripheral blood leukocytes, LPS receptor may be associated with leukemia.
在本研究中，我们观察到溶血磷脂酰丝氨酸（LPS）刺激白血病细胞内的细胞内钙（Ca(2+)）增加，但对正常人外周血单个核细胞无此作用。LPS也刺激人白血病THP-1细胞内的Ca(2+)增加。LPS刺激引起的Ca(2+)增加被U-73122抑制，但不被U-73343抑制。LPS还刺激THP-1细胞中肌醇磷酸的形成，提示LPS通过磷脂酶C激活刺激钙信号传导。此外，百日咳毒素（PTX）完全抑制LPS引起的Ca(2+)增加，表明PTX敏感的G蛋白被激活。我们还发现苏拉明完全抑制LPS诱导的Ca(2+)增加，提示G蛋白偶联受体被激活。由于LPS特异性刺激PTX敏感的G蛋白、白血病细胞中依赖磷脂酶C的Ca(2+)增加而不刺激正常外周血白细胞，LPS受体可能与白血病相关。
