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Zinc accumulation in mitochondria promotes ischemia-induced BBB disruption through Drp1-dependent mitochondria

Zhifeng Qi1, Wenjuan Shi1, Yongmei Zhao1

  • 1Department of Neurology, Cerebrovascular Diseases Research Institute, Xuanwu hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, China.

Toxicology and Applied Pharmacology
|June 2, 2019
PubMed

Insights

Mitochondrial zinc overload increases reactive oxygen species (ROS) and disrupts the blood-brain barrier (BBB) after ischemia. This zinc-ROS pathway in mitochondria contributes to BBB disruption via mitochondrial fission.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • High zinc concentrations can cause neuronal death in ischemic brains.
  • Labile zinc accumulation in cerebromicrovessels increases blood-brain barrier (BBB) permeability post-ischemia.
  • The specific role of mitochondrial zinc in ischemia-induced BBB changes remains unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial zinc in ischemia-induced BBB permeability alterations.
  • To elucidate the mechanisms by which zinc affects endothelial cells and mitochondria during ischemia/reperfusion.

Main Methods:

  • Studied free zinc accumulation and reactive oxygen species (ROS) generation in cultured endothelial cells (ECs) and isolated brain microvessels from ischemic rats.
  • Analyzed mitochondrial zinc accumulation, ROS generation, and mitochondrial morphology.
  • Investigated the involvement of Dynamin-related protein-1 (Drp-1) and matrix metalloproteinase-2 (MMP-2) in zinc-induced mitochondrial changes and BBB permeability.

Main Results:

  • Ischemia/reperfusion led to free zinc accumulation in ECs, increasing ROS generation.
  • Zinc accumulated significantly in mitochondria, causing mitochondrial ROS generation and collapse of mitochondrial networks via Drp-1 dependent fission.
  • Mitochondrial zinc overload activated MMP-2, contributing to BBB permeability increase.

Conclusions:

  • Mitochondrial zinc overload is a key factor in ischemia-induced BBB disruption.
  • The zinc-ROS pathway within mitochondria, involving Drp-1 dependent mitochondrial fission, mediates BBB damage.
  • Targeting mitochondrial zinc may offer a therapeutic strategy for stroke-related brain injury.
Keywords:
Blood–Brain Barrier (BBB)FissionIschemia/reperfusionMitochondriaReactive Oxygen Species (ROS)Zinc

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