溶血磷脂酰胆碱刺激脑微血管平滑肌细胞增殖的细胞内信号转导途径

通过测定［³H］胸腺嘧啶核苷(［³H］TdR)参入和结晶紫染色法测定平滑肌细胞增殖，研究了溶血磷脂酰胆碱(LPC)刺激牛脑微血管平滑肌细胞(BCMSMC)增殖的细胞内信号转导途径. 结果显示，LPC能浓度依赖性(1 nmol·L^-1-10 μmol·L^-1)诱导BCMSMC摄取［³H］TdR，在LPC的浓度为10 μmol·L^-1时作用达最大，cpm由366±142升至1761±296(P<0.01)；LPC亦能浓度依赖性(1 nmol·L^-1-10 μmol·L^-1)诱导BCMSMC增殖，在LPC浓度为1 μmol·L^-1时促增殖作用达坪值，A_{595 nm}由0.060±0.009增至0.100±0.015(P<0.01). 丝裂原激活蛋白激酶(MAPK)特异性抑制剂PD 98059(2-50 μmol·L^-1)，血小板衍生生长因子受体抑制剂酪氨酸磷酸化抑制剂AG 1296(2-50 μmol·L^-1)以及蛋白质酪氨酸激酶抑制剂除莠霉素A(2-10 μmol· L^-1)能浓度依赖性地抑制LPC的上述作用. 表明LPC能促进BCMSMC增殖，其细胞内信号转导与MAPK途径有关.

ignal transduction pathways stimulated by lysophosphatidylcholine in cultured bovine cerebral microvascular smooth muscle cells

The signal transduction pathways stimulated by lysophosphatidylcholine (LPC) in bovine cerebral microvascular smooth muscle cells (BCMSMC) were studied. The ［³H］TdR incorporation and crystal violet assay were measured in BCMSMC. The results showed that LPC enhanced the BCMSMC ［³H］TdR incorporation in a concentration (1 nmol·L^-1-10 μmol·L^-1)- dependent manner. At 10 μmol·L^-1, the incorporation rate reached maximum (cpm from 366±142 to 1761±296, P<0.01); LPC also promoted the proliferation of BCMSMC in a concentration (1 nmol·L^-1-10 μmol·L^-1) dependent manner. At 1 μmol·L^-1, the effect reached plateau level (A_{595 nm} from 0.060±0.009 to 0.100±0.015). Mitogen-activated protein kinase (MAPK) inhibitor PD 98059 (2-50 μmol·L^-1), platelet derived growth factor receptor inhibitor tyrphostin AG 1296 (2-50 μmol·L^-1) and protein tyrosine kinase inhibitor herbimycin A (2-10 μmol·L^-1) inhibited the BCMSMC ［³H］TdR incorporation and proliferation of BCMSMC. The data indicate that LPC may stimulate the proliferation of BCMSMC. The LPC-induced intracellular signal transduction may be related to the MAPK pathway.