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Unraveling the Role of α2δ-1 in Cerebral Hemorrhage: Calcium Overload, Endoplasmic Reticulum Stress, and Microglial

Ning Yu1, Xiaopeng Li2, Bingqian Wang3

  • 1Department of Anesthesiology and intensive care unit, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China.

Brain and Behavior
|May 7, 2025
PubMed

Insights

Dysregulated α2δ-1 protein contributes to cerebral hemorrhage by increasing calcium levels, endoplasmic reticulum stress, and microglia apoptosis. Targeting α2δ-1 may offer new therapeutic strategies for brain injury.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Cerebral hemorrhage is a critical neurological condition with significant mortality.
  • Understanding the molecular mechanisms of cerebral hemorrhage is vital for developing treatments.

Purpose of the Study:

  • To investigate the role of the α2δ-1 protein in the pathogenesis of cerebral hemorrhage.
  • To explore the impact of α2δ-1 dysregulation on calcium signaling and cellular stress pathways.

Main Methods:

  • Observed α2δ-1 expression in cerebral hemorrhage tissue.
  • Utilized α2δ-1 knockdown in BV2 microglia to assess effects on calcium concentration, protein phosphorylation (PLCr, IP3R), and endoplasmic reticulum stress (ERS).
  • Analyzed apoptosis-related proteins and ERS markers (PERK).

Main Results:

  • Significant upregulation of α2δ-1 was found in cerebral hemorrhage tissue.
  • Knockdown of α2δ-1 reduced intracellular calcium, decreased PLCr and IP3R phosphorylation, and mitigated ERS in BV2 microglia.
  • α2δ-1 knockdown inhibited BV2 microglia apoptosis and downregulated associated proteins.

Conclusions:

  • α2δ-1 is implicated in calcium-mediated signaling, endoplasmic reticulum stress, and microglia apoptosis in cerebral hemorrhage.
  • The findings suggest α2δ-1 as a potential therapeutic target for cerebral hemorrhage and associated secondary brain injuries.
Abstract

Keywords:
calcium signalingcerebral hemorrhage endoplasmic reticulum stressα2δ‐1

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