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Nr1d1 Mediates Microglial Inflammatory Activation Induced by Intermittent Hypoxia: A Transcriptomic and Machine

Zhuoran Sun1,2, Tengqun Shen1, Mengfan Li1

  • 1Department of Neurology, Weihai Municipal Hospital, Shandong University, Jinan, Shandong, China.

Journal of Molecular Neuroscience : MN
|July 11, 2026
PubMed
Summary

Obstructive sleep apnea causes intermittent hypoxia, leading to brain inflammation. This study identifies Nr1d1 as a key gene involved in microglial activation during this process.

Keywords:
Intermittent hypoxiaMachine learningMicrogliaNeuroinflammationNr1d1RNA sequencing

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Obstructive sleep apnea (OSA) involves recurrent intermittent hypoxia (IH), a known contributor to neuroinflammation and neurological deficits.
  • Microglia, the brain's immune cells, play a crucial role in inflammatory responses, but the specific molecular pathways activated by IH are not fully understood.

Purpose of the Study:

  • To identify key genes mediating microglial activation under IH conditions.
  • To investigate the functional significance of these genes in IH-induced neuroinflammation.

Main Methods:

  • An in vitro model of IH was established using BV2 microglial cells.
  • Inflammation markers (COX2, iNOS, IL-6, TNF-α) were measured using Western blot and ELISA.
  • RNA sequencing was employed to analyze transcriptional changes.
  • Bioinformatic analyses including differential expression, enrichment, network, and machine learning were performed.
  • Pharmacological inhibition of candidate gene Nr1d1 was used to assess its role.

Main Results:

  • IH significantly elevated inflammatory markers (COX2, iNOS, IL-6, TNF-α) in BV2 cells.
  • Transcriptomic profiling revealed distinct gene expression patterns between control and IH conditions.
  • Network analysis identified a cluster of circadian genes, including Nr1d1, as central to IH-responsive transcriptional changes.
  • Inhibition of Nr1d1 demonstrably reduced IH-induced inflammatory responses in microglial cells.

Conclusions:

  • Intermittent hypoxia triggers significant inflammatory activation and transcriptional reprogramming in microglial cells.
  • Nr1d1 emerges as a potential key regulator, linking circadian rhythms to microglial inflammatory activation in the context of IH.
  • Targeting Nr1d1 may offer a therapeutic strategy for mitigating neuroinflammation associated with obstructive sleep apnea.