17β-estradiol upregulates striatin protein levels via Akt pathway in human umbilical vein endothelial cells

PLoS One. 2018 Aug 23;13(8):e0202500. doi: 10.1371/journal.pone.0202500. eCollection 2018.

Abstract

17β-estradiol (E2) has been shown to have beneficial effects on the cardiovascular system. We previously demonstrated that E2 increases striatin levels and inhibits migration in vascular smooth muscle cells. The objective of the present study was to investigate the effects of E2 on the regulation of striatin expression in human umbilical vein endothelial cells (HUVECs). We demonstrated that E2 increased striatin protein expression in a dose- and time-dependent manner in HUVECs. Pretreatment with ICI 182780 or the phosphatidylinositol-3 kinase inhibitor, wortmannin, abolished E2-mediated upregulation of striatin protein expression. Treatment with E2 resulted in Akt phosphorylation in a time-dependent manner. Moreover, silencing striatin significantly inhibited HUVEC migration, while striatin overexpression significantly promoted HUVEC migration. Finally, E2 enhanced HUVEC migration, which was inhibited by silencing striatin. In conclusion, our results demonstrated that E2-mediated upregulation of striatin promotes cell migration in HUVECs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calmodulin-Binding Proteins / biosynthesis*
  • Cell Movement / drug effects
  • Estradiol / pharmacology*
  • Fulvestrant / pharmacology
  • Human Umbilical Vein Endothelial Cells / cytology
  • Human Umbilical Vein Endothelial Cells / metabolism*
  • Humans
  • Membrane Proteins / biosynthesis*
  • Nerve Tissue Proteins / biosynthesis*
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*
  • Up-Regulation / drug effects*

Substances

  • Calmodulin-Binding Proteins
  • Membrane Proteins
  • Nerve Tissue Proteins
  • STRN protein, human
  • Fulvestrant
  • Estradiol
  • Proto-Oncogene Proteins c-akt

Grants and funding

This study was supported by the National Natural Science Foundation of China (Grant No. 81774107 to J.W.X.), Department of Education of Guangdong Province (Grant No. yq2014045 to J.W.X.), Guangzhou University of Chinese Medicine (Grant No. QNYC20170101 to J.W.X.), by the Guangdong Natural Science Foundation (Grant No. 2014A030310059 to S.Z. and Grant No. 2014A030313105 to Y.X.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.