Mitochondria-associated endoplasmic reticulum membrane as a mediator of vanadium-induced endoplasmic reticulum

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Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)
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Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

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Yiqun Lin1, Fan Yang1, Xueyan Dai1

  • 1Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang, 330045, Jiangxi, People's Republic of China.

Environmental Science and Pollution Research International
|March 6, 2024
PubMed

Insights

Excess vanadium exposure disrupts brain mitochondria-associated endoplasmic reticulum membrane (MAM) integrity and activates endoplasmic reticulum quality control (ERQC) pathways, leading to cellular damage. This study reveals vanadium

Area of Science:

  • Neurotoxicology
  • Cellular Biology
  • Trace Element Research

Background:

  • Vanadium (V) is essential for normal cellular function but toxic in excess, particularly affecting the brain.
  • Mitochondria-associated endoplasmic reticulum membrane (MAM) is crucial for endoplasmic reticulum quality control (ERQC) and cellular homeostasis.
  • Understanding the impact of excess vanadium on MAM and ERQC in the brain is vital for neurotoxicity research.

Purpose of the Study:

  • To investigate the effects of excessive vanadium exposure on MAM integrity and ERQC in the duck brain.
  • To analyze the molecular mechanisms underlying vanadium-induced neurotoxicity.
  • To evaluate the relationship between vanadium exposure, MAM disruption, and ERQC activation.

Main Methods:

  • Histomorphological analysis of brain tissues from control and vanadium-exposed ducks.
  • Determination of trace element content in brain tissues.
  • Quantitative analysis of mRNA and protein expression for MAM, ERQC, and autophagy-related factors.

Main Results:

  • Excess vanadium exposure led to trace element imbalance and disrupted MAM integrity in duck brains.
  • Vanadium exposure caused endoplasmic reticulum rupture and induced autophagosome formation.
  • IP3R and VDAC1 co-localization was inhibited, MAM-related factors were downregulated, while ERQC and autophagy factors were upregulated.

Conclusions:

  • Excess vanadium exposure disrupts brain MAM integrity and activates ERQC pathways.
  • The observed disruption and activation contribute to vanadium-induced neurotoxicity and subsequent autophagy.
  • This study highlights the critical role of MAM and ERQC in vanadium neurotoxicity.
Keywords:
AutophagyBrainEndoplasmic reticulum quality controlMitochondria-associated endoplasmic reticulum membraneVanadium

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