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Poly(ADP-ribose) polymerase-1 regulates microglia mediated decrease of endothelial tight junction integrity.

Abbas Rezaeian Mehrabadi1, Minna A Korolainen2, Gary Odero1

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Summary

Alzheimer's disease pathology involves microglia that damage the blood-brain barrier (BBB). Inhibiting poly(ADP-ribose) polymerase-1 (PARP-1) in microglia prevents amyloid-beta-induced BBB disruption, offering a potential therapeutic strategy.

Keywords:
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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Alzheimer's disease (AD) is characterized by neuronal damage, reactive gliosis, and compromised blood-brain barrier (BBB) integrity.
  • Microglia, the brain's immune cells, are closely linked to the BBB, and their pro-inflammatory responses during AD may exacerbate BBB damage.

Purpose of the Study:

  • To investigate the direct impact of amyloid-beta (Aβ)-stimulated microglia on BBB integrity using co-culture models.
  • To determine if modulating microglial phenotype via poly(ADP-ribose) polymerase-1 (PARP-1) inhibition can reverse microglial-induced BBB damage.

Main Methods:

  • Co-culture of primary murine microglia with mouse brain endothelial cells (bEnd3) and murine astrocytes.
  • Assessment of tight junction protein (TJP) expression (ZO-1, occludin) in endothelial cells.
  • Measurement of glial fibrillary acidic protein (GFAP) in astrocytes.
  • Analysis of microglial nitric oxide (NO) and tumor necrosis factor alpha (TNFα) release.
  • Evaluation of PARP-1 inhibition effects on microglial responses and BBB integrity.

Main Results:

  • Unstimulated microglia enhanced TJP expression, while Aβ-stimulated microglia reduced ZO-1 and occludin levels in endothelial cells.
  • Aβ-stimulated microglia increased GFAP expression in co-cultured astrocytes, indicating astrogliosis.
  • Aβ induced microglial release of NO and TNFα, leading to decreased TJP expression, increased endothelial permeability, and astrogliosis.
  • PARP-1 inhibition in microglia attenuated Aβ-induced BBB damaging effects.

Conclusions:

  • PARP-1-mediated microglial responses, including NO and TNFα release, directly impair BBB integrity by degrading TJPs, increasing permeability, and inducing astrogliosis.
  • PARP-1 acts as a key modulator of microglial phenotype, and its inhibition can prevent microglial-driven BBB damage.
  • Targeting microglial PARP-1 presents a potential therapeutic strategy for mitigating BBB dysfunction in Alzheimer's disease.