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Updated: Feb 13, 2026

Optimized Transfection Strategy for Expression and Electrophysiological Recording of Recombinant Voltage-Gated Ion Channels in HEK-293T Cells
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Optimized Transfection Strategy for Expression and Electrophysiological Recording of Recombinant Voltage-Gated Ion Channels in HEK-293T Cells

Published on: January 19, 2011

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Deficiency of voltage-gated proton channel Hv1 attenuates streptozotocin-induced β-cell damage

Xudong Wang1, Wang Xi1, Jiwei Qin1

  • 1Department of Biophysics, School of Physical Science, The Key Laboratory of Bioactive Materials, Ministry of Education, Nankai University, Tianjin 300071, PR China.

Biochemical and Biophysical Research Communications
|March 19, 2018
PubMed

Insights

The voltage-gated proton channel Hv1 contributes to diabetes by increasing reactive oxygen species (ROS) in pancreatic cells. Inhibiting Hv1 protects against STZ-induced diabetes and beta-cell damage.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Reactive oxygen species (ROS) are implicated in pancreatic beta-cell dysfunction and diabetes development.
  • Streptozotocin (STZ) induces beta-cell dysfunction through ROS production.
  • The voltage-gated proton channel Hv1 is crucial for ROS production by providing charge compensation.

Purpose of the Study:

  • To investigate the role of Hv1 in STZ-induced pancreatic beta-cell damage.
  • To determine if Hv1 deficiency protects against STZ-induced diabetes.

Main Methods:

  • Utilized a mouse model deficient in Hv1.
  • Administered STZ to induce diabetes.
  • Assessed glucose intolerance, beta-cell mass, insulin content, and ROS production.

Main Results:

  • Hv1 deficiency significantly inhibited STZ-induced glucose intolerance in mice.
  • Loss of Hv1 prevented STZ-induced reduction in beta-cell mass and insulin content.
  • Hv1 deficiency markedly attenuated STZ-induced beta-cell damage and ROS production.

Conclusions:

  • Hv1 plays a significant role in STZ-induced pancreatic beta-cell damage and ROS generation.
  • Targeting Hv1 may represent a therapeutic strategy for preventing or treating diabetes associated with ROS production.
Keywords:
DamageDiabetesHv1Pancreatic β-cellsROSVoltage-gated proton channel

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