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Related Concept Videos

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Related Experiment Video

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The Use of Mouse Splenocytes to Assess Pathogen-associated Molecular Pattern Influence on Clock Gene Expression
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The intrinsic microglial clock system regulates interleukin-6 expression.

Ryota Nakazato1,2, Shogo Hotta1, Daisuke Yamada1,3

  • 1Division of Pharmaceutical Sciences, Laboratory of Molecular Pharmacology, Kanazawa University Graduate School, Kanazawa, Ishikawa, 920-1192, Japan.

Glia
|October 12, 2016
PubMed
Summary

Microglia possess an internal molecular clock that regulates inflammatory responses. The Brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (Bmal1) clock gene is crucial for controlling interleukin-6 (IL-6) production in microglia during inflammation and brain injury.

Keywords:
Bmal1IL-6clock genesmicroglia

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Area of Science:

  • Neuroimmunology
  • Chronobiology
  • Molecular Biology

Background:

  • Microglia, the brain's resident immune cells, possess intrinsic molecular clocks, similar to neurons.
  • The master clock gene Brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (Bmal1) influences microglial inflammatory responses, including interleukin-6 (IL-6) production.

Purpose of the Study:

  • To investigate the mechanisms by which microglial molecular clock components regulate pro-inflammatory cytokine production.
  • To determine the role of Bmal1 in lipopolysaccharide (LPS)-induced IL-6 expression and its impact on brain injury.

Main Methods:

  • Utilized microglial cell lines (BV-2) and primary microglia from Per1::Luciferase transgenic and Bmal1-deficient mice.
  • Employed siRNA targeting Bmal1, pharmacological inhibition with SR9011, and promoter analysis of the Il6 gene.
  • Investigated Bmal1's role in a mouse model of middle cerebral artery occlusion (MCAO).

Main Results:

  • Clock gene transcripts and luciferase activity exhibited diurnal rhythmicity in microglia.
  • siRNA-mediated Bmal1 knockdown and Bmal1 deficiency selectively inhibited LPS-induced IL-6 expression.
  • Pharmacological disruption of circadian rhythmicity and Bmal1 deficiency in microglia attenuated IL-6 upregulation and neuronal damage following MCAO.

Conclusions:

  • The intrinsic microglial molecular clock, particularly Bmal1, positively regulates IL-6 expression.
  • Bmal1 plays a critical role in modulating microglial inflammatory responses during pathological conditions like stroke.
  • Targeting the microglial clock may offer therapeutic strategies for neuroinflammatory diseases.