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高糖激活WNT信号通路促进血管平滑肌细胞钙化

颜建云 周芹 于汇民 侯梦琳 陆立鹤

南方医科大学学报Issue(1):29-33,5.
南方医科大学学报Issue(1):29-33,5.DOI:10.3969/j.issn.1673-4254.2015.01.06

高糖激活WNT信号通路促进血管平滑肌细胞钙化

High glucose promotes vascular smooth muscle cell calcification by activating WNT signaling pathway

颜建云 1周芹 2于汇民 3侯梦琳 4陆立鹤4

作者信息

  • 1. 南方医科大学基础医学院组织胚胎学教研室,广东 广州 510515
  • 2. 中山大学 附属第一医院麻醉科,广东 广州 510080
  • 3. 广东省人民医院心内科//广东省医学科学院广东省心血管病研究所,广东 广州 510080
  • 4. 中山大学 中山医学院病理生理学教研室,广东 广州 510080
  • 折叠

摘要

Abstract

Objective To investigate whether high glucose-induced vascular calcification is associated with WNT signaling pathway. Methods An in vitro model of human vascular smooth muscle cell (VSMC) calcification was induced by exposure of the cells to high glucose. The expressions of WNT signal molecules and bone-related proteins including Cbfa1, Osx, OCN and BMP2 were analyzed with qRT-PCR, and the cell calcification was assessed by alizarin red staining. The effect of Dkk1, a WNT signaling inhibitor, on high glucose-induced cell calcification was tested with alizarin red staining and calcium content analysis. Results High glucose activated WNT signaling pathway in human VSMCs by up-regulating the expressions of WNT signal molecules including Wnt3a, Wnt7a, Fzd4 and Wisp1 mRNA by 1.86, 1.68, 2.1, and 2.3 folds, respectively, and by promoting the phosphorylation ofβ-catenin (2.70±0.22, P<0.05), a key mediator of WNT signaling pathway. Inhibition of WNT signaling pathway by Dkk1 attenuated high glucose-induced VSMC calcification and down-regulated the expression of bone-related proteins Cbfa1, Osx, OCN, and BMP2 by (51 ± 9)%, (58 ± 11)%, (56 ± 10)%, and (62 ± 10)% (P<0.01). Conclusion WNT signaling pathway is involved in high glucose-induced VSMC calcification.

关键词

血管钙化/WNT/高糖/β-catenin/血管平滑肌细胞

Key words

vascular calcification/WNT/high glucose/β-catenin/vascular smooth muscle cells

引用本文复制引用

颜建云,周芹,于汇民,侯梦琳,陆立鹤..高糖激活WNT信号通路促进血管平滑肌细胞钙化[J].南方医科大学学报,2015,(1):29-33,5.

基金项目

国家自然科学基金(81000124,81470488);中山大学高校基本科研业务费专项资金(11ykpy8);教育部留学回国人员科研启动基金资助项目Supported by National Natural Science Foundation of China (81000124,81470488) (81000124,81470488)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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