Affordable Access

Access to the full text

Hypoxia induces the translocation of glucose transporter 1 to the plasma membrane in vascular endothelial cells

Authors
  • Mamun, Abdullah Al1, 2
  • Hayashi, Hisaki1
  • Yamamura, Aya1
  • Nayeem, Md Junayed1
  • Sato, Motohiko1
  • 1 Aichi Medical University, 1-1 Yazako-Karimata, Nagakute-City, Aichi, 4801165, Japan , Nagakute-City, Aichi (Japan)
  • 2 Mawlana Bhashani Science and Technology University, Santosh, Tangail, 1902, Bangladesh , Santosh, Tangail (Bangladesh)
Type
Published Article
Journal
The Journal of Physiological Sciences
Publisher
BioMed Central
Publication Date
Sep 22, 2020
Volume
70
Issue
1
Identifiers
DOI: 10.1186/s12576-020-00773-y
Source
Springer Nature
Keywords
License
Green

Abstract

Glucose uptake and adenosine triphosphate (ATP) generation are important for the survival and growth of endothelial cells. An increase of glucose uptake under hypoxia was previously shown to be associated with the increased expression of glucose transporters (GLUTs). However, the regulation of GLUT trafficking to the cell surface has not been examined in detail. Here, we report the characterization of GLUT1 translocation to the plasma membrane during hypoxia in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were exposed to hypoxia (1% O2) for 12 h, which significantly induced GLUT1 expression and translocation to the plasma membrane. GLUT1 translocation was associated with a decrease of intracellular ATP by hypoxia. Decreasing ATP levels with antimycin-A and 2-deoxyglucose induced GLUT1 translocation under normoxia. The induction of hypoxia-inducible factor-1α under normoxia did not influence the cell surface expression of GLUT1 or cellular ATP concentration. Interestingly, the translocation of GLUT1 induced by hypoxia was inhibited by the ATP-sensitive potassium (KATP) channel inhibitor glibenclamide, while the mitochondrial KATP channel inhibitor 5-HD did not influence GLUT1 translocation during hypoxia. These observations indicate that a decrease of intracellular ATP triggers GLUT1 translocation to the plasma membrane and is mediated by KATP channels, which would contribute to glucose uptake in HUVECs during hypoxia.

Report this publication

Statistics

Seen <100 times