基础医学与临床 ›› 2013, Vol. 33 ›› Issue (10): 1284-1287.

• 研究论文 • 上一篇    下一篇

Wnt信号参与氯化锂下调低氧复氧诱导HUVEC表达趋化因子FKN

殷菱1,李法琦2,周平3,曾德康4   

  1. 1. 四川省泸州医学院
    2. 重庆医科大学
    3. 重庆医科大学附属第一医院老年科
    4. 重钢总医院老年科
  • 收稿日期:2012-09-21 修回日期:2013-01-28 出版日期:2013-10-05 发布日期:2013-09-25
  • 通讯作者: 李法琦 E-mail:faqili-2006@yahoo.com.cn

Wnt signaling takes part in down-regulation of hypoxia-induced fractalkine expression with LiCl in HUVECs

  • Received:2012-09-21 Revised:2013-01-28 Online:2013-10-05 Published:2013-09-25

摘要: 目的 研究低氧复氧诱导的培养的人脐静脉内皮细胞(HUVECs)表达趋化因子FKN与Wnt信号通路中关键信号分子β-catenin、GSK-3β的相关性。方法 HUVECs,随机分为对照组、低氧复氧组和氯化锂(LiCl, 10mmol/L)组。免疫细胞荧光FITC 法检测FKN蛋白表达,免疫细胞化学技术检测GSK-3β及β-catenin的表达。RT-PCR技术检测GSK-3β和FKN mRNA表达。结果 与正常对照组比较,低氧复氧引起GSK-3β、β-catenin及FKN表达明显增加(P<0.05),于复氧2h达表达高峰;与低氧复氧组比较,LiCl组β-catenin表达明显增加(P<0.05),FKN与GSK-3β表达明显降低(P<0.05),但仍然高于正常对照组。LiCl组FKNmRNA表达高于正常对照组(P<0.05)而低于低氧复氧组(P<0.05),于复氧1h达表达高峰;GSK-3βmRNA在低氧前后及复氧各时间点无差异表达。结论 Wnt信号通路的激活可能在转录后翻译阶段参与LiCl下调低氧诱导HUVECs表达FKN的过程。

关键词: 低氧复氧, 人脐静脉内皮细胞, FKN, Wnt信号

Abstract: Objective To investigate the relationship between Wnt signaling pathway and hypoxia -induced fractalkine expression in human umbilical vein endothelial cells. Methods HUVECs were cultivated and divided into three groups randomly (control group, hypoxia/reoxygenation group, LiCl 10mmol/L group), which were used to establish the hypoxia/reoxygenation models. The mRNA expressions of fractalkine and GSK-3β were assessed by RT-PCR. The intracellular distribution and expression of fractalkine were determined by immunofluorescent staining. The expression of GSK-3β and β-catenin were analyzed with immunocytochemistry. Results Compared with control group, in hypoxia/reoxygenation group, the expression of GSK-3β and β-catenin were increased (P<0.05), the mRNA and protein expression of fractalkine increased remarkably (P<0.05). Compared with hypoxia/reoxygenation group, in LiCl groups, the mRNA and protein expression of fractalkine reduced significantly (P<0.05), the expression of GSK-3β reduced but β-catenin increased relativitily (P<0.05). However, the mRNA expression of GSK-3β had no statistically difference in all groups. Conclusion The hypoxia induced the damage of HUVECs through upregulating fractalkine expression. LiCl pretreatment inhibited fractalkine expression proportional. Its mechanism may be related to the activation of Wnt signaling pathway.

Key words: hypoxia/reoxygenation, human umbilical vein endothelial cells, fractalkine, Wnt signaling pathway

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