• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>RSC Advances >Zn(ii)2,9-dimethyl-1,10-phenanthroline stimulates cultured bovine aortic endothelial cell proliferation
【24h】

Zn(ii)2,9-dimethyl-1,10-phenanthroline stimulates cultured bovine aortic endothelial cell proliferation

机译：Zn（ii）2,9-二甲基-1,10-菲咯啉刺激培养的牛主动脉内皮细胞增殖

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Vascular endothelial cells cover the luminal surface of blood vessels in a monolayer. Proliferation of these cells is crucial for the repair of damaged endothelial monolayers. In the present study, we identified a zinc complex, Zn( II )2,9-dimethyl-1,10-phenanthroline (Zn-12), that stimulates the proliferation of bovine aortic endothelial cells in a culture system. No such stimulatory activity was observed for the ligand alone or in combination with other metals; however, the ligand combined with iron weakly stimulated the proliferation, as evidenced by the [ ~(3) H]thymidine incorporation assay. Inorganic zinc weakly but significantly stimulated proliferation, and intracellular accumulation of zinc was similar between inorganic zinc and Zn-12 treatment, suggesting that the mechanisms by which Zn-12 stimulates vascular endothelial cell proliferation contain processes that differ from those by which inorganic zinc stimulates proliferation. Although expression of endogenous fibroblast growth factor-2 (FGF-2) and its receptor FGFR-1 was unchanged by Zn-12, both siRNA-mediated knockdown of FGF-2 and FGFR inhibition partly but significantly suppressed the stimulation of vascular endothelial cell proliferation by Zn-12, indicating that the zinc complex activates the FGF-2 pathway to stimulate proliferation. Phosphorylation of ERK1/2 and MAPKs was induced by Zn-12, and PD98059, a MEK1 inhibitor, significantly suppressed the stimulatory effect of Zn-12 on vascular endothelial cell proliferation. Therefore, it is suggested that Zn-12 activates the FGF-2 pathway via activation of ERK1/2 signaling to stimulate vascular endothelial cell proliferation, although FGF-2-independent mechanisms are also involved in the stimulation. Zn-12 and related compounds may be promising molecular probes to analyze biological systems of vascular endothelial cells.
机译：血管内皮细胞在单层中覆盖血管的腔表面。这些细胞的增殖对于修复受损内皮单层来说至关重要。在本研究中，我们鉴定了锌络合物，Zn（II）2,9-二甲基-1,10-菲啉（Zn-12），其刺激培养系统中牛主动脉内皮细胞的增殖。单独的配体或与其他金属组合没有观察到这种刺激活性;然而，配体与铁弱刺激增殖，如[〜（3）H]胸苷掺入测定。无机锌弱但显着刺激的增殖，锌的细胞内积聚在无机锌和Zn-12处理之间相似，Zn-12刺激血管内皮细胞增殖的机制含有与无机锌刺激增殖的过程不同的方法。虽然通过Zn-12表达内源性成纤维细胞生长因子-2（FGF-2）及其受体FGFR-1，但部分介导的FGF-2和FGFR抑制的SiRNA介导的敲低，部分但显着抑制了血管内皮细胞增殖的刺激通过Zn-12，表明锌复合物激活FGF-2途径以刺激增殖。 ERK1 / 2和MAPK的磷酸化由Zn-12和MeK1抑制剂PD98059诱导，显着抑制了Zn-12对血管内皮细胞增殖的刺激作用。因此，建议Zn-12通过激活ERK1 / 2信号传导来激活FGF-2途径，以刺激血管内皮细胞增殖，尽管FGF-2独立机制也参与刺激。 Zn-12和相关化合物可能是对分析血管内皮细胞的生物学系统的有前途的分子探针。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号