摘要
目的研究趋化因子受体CCR7对成熟树突状细胞(DCs)的抗凋亡作用,并对其机制进行探讨。方法体外培养大鼠骨髓来源DCs,脂多糖诱导成熟。加入CCR7配体CCL21进行刺激,以不加CCL21为对照组,流式细胞术检测细胞凋亡率,Western blot检测磷酸化Akt、Akt蛋白表达,应用Wortmannin抑制PI3K/Akt信号通路进一步观察磷酸化Akt蛋白表达和细胞凋亡的变化。结果在CCL21的作用下,DCs细胞凋亡率明显低于对照组,而磷酸化Akt蛋白表达却明显增高(P<0.05)。DCs经PI3K抑制剂预处理后,CCR7介导的Akt蛋白磷酸化及抗凋亡作用被阻断。结论在CCL21作用下,CCR7介导了抗凋亡效应,其对DCs的凋亡调控通过PI3K/Akt信号通路发挥作用。
Objective To investigate the anti-apoptotic mechanism of mature dendritic cells （DCs） mediated by CCR7. Methods Cells isolated from rat bone marrow were induced to differentiate to DCs and cultured for 7 days, then LPS was added for other 48 h to induce maturation of the cells. The percentage of apoptosis and expression of phosphorylated Akt and total Akt proteins in muture DCs were measured in the presence or absence of CCL21 by flow cytometry and Western blot respectively. Wortmannin was used to inhibit the PI3K/Akt signaling pathway for further observing changes in the expression of phosphorylated Akt protein and apoptosis. Results In CCL21-treated DCs, the percentage of apoptosis was significantly lower and the expression of phosphorylated Akt protein significantly higher than in control group （P〈0.05）. Pretreatment of DCs with wortmannin abrogated the phoshorylation of Akt protein and anti-apoptotic effects mediated by CCR7. Conclusion Stimulation of CCR7 mediates the anti-apoptotic effects of mature DCs via PI3K/Akt signaling pathway.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2007年第4期469-471,共3页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
