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Lead inhibits microglial cell migration via suppression of store-operated calcium entry

Wei Tang1, Jiawen Peng1, Lixuan Chen1

  • 1Department of Occupational Health and Occupational Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, Guangdong, China; Department of Occupational & Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.

Toxicology Letters
|January 28, 2024
PubMed

Insights

Lead exposure inhibits microglial migration, a key feature of neuroinflammation. This occurs by downregulating store-operated calcium entry (SOCE) and impairing STIM1 function, impacting brain health.

Area of Science:

  • Neuroscience
  • Environmental Toxicology
  • Cell Biology

Background:

  • Lead (Pb) is a persistent environmental pollutant linked to neurotoxicity and neuroinflammation.
  • Microglial activation is central to neuroinflammation, with migration being a critical cellular function.
  • The specific impact of lead on microglial migration remains largely unknown.

Purpose of the Study:

  • To investigate the effect of lead (Pb) exposure on microglial migration.
  • To elucidate the underlying mechanisms, focusing on calcium signaling pathways.

Main Methods:

  • Utilized BV-2 microglial cell lines and primary microglial cells.
  • Assessed microglial activation markers (TNF-α, CD206) post-Pb treatment.
  • Measured store-operated calcium entry (SOCE) and CRAC currents.
  • Analyzed protein levels of STIM1, STIM2, and Orai1.
  • Investigated rescue effects via STIM1 overexpression.

Main Results:

  • Pb treatment increased microglial activation markers (TNF-α, CD206).
  • Lead significantly inhibited microglial migration ability.
  • Pb exposure dose-dependently downregulated SOCE and CRAC currents.
  • No significant changes were observed in STIM1, STIM2, or Orai1 protein levels.
  • Overexpression of STIM1 or its CRAC activation domain partially restored calcium influx and migration.

Conclusions:

  • Lead (Pb) inhibits microglial migration.
  • This inhibition is mediated by the downregulation of store-operated calcium entry (SOCE).
  • Impairment of STIM1 function plays a crucial role in Pb-induced inhibition of microglial migration.
Keywords:
LeadMicrogliaMigrationNeuroinflammationStore-operated calcium entry

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