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Translocator Protein 18 kDa (TSPO) Deficiency Inhibits Microglial Activation and Impairs Mitochondrial Function

Rumeng Yao1,2, Ruiyuan Pan3, Chao Shang4

  • 1Department of Neuropharmacology and Drug Discovery, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China.

Frontiers in Pharmacology
|July 23, 2020
PubMed

Insights

Translocator protein (TSPO) is crucial for microglial activation and central nervous system (CNS) neuroinflammation. TSPO deficiency impairs microglial metabolism, offering a potential therapeutic target for CNS diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Translocator protein (TSPO) is upregulated in activated microglia within the central nervous system (CNS).
  • The precise role and regulatory mechanisms of TSPO in microglial activation remain incompletely understood.

Purpose of the Study:

  • To elucidate the function and mechanism of TSPO in microglial activation.
  • To investigate the impact of TSPO deficiency on microglial metabolic function.

Main Methods:

  • Primary microglia were isolated from TSPO knockout mice.
  • A TSPO-knockdown microglial cell line was established.
  • Microglial activation was induced using lipopolysaccharide (LPS) or IL-4.
  • Mitochondrial membrane potential, ATP production, and cellular energy metabolism (OXPHOS and glycolysis) were analyzed.

Main Results:

  • TSPO deficiency significantly attenuated LPS- or IL-4-induced microglial activation.
  • TSPO deficiency led to reduced mitochondrial membrane potential and ATP production.
  • TSPO deficiency suppressed mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis, causing metabolic deficits in microglia.

Conclusions:

  • TSPO plays a critical role in microglial activation by regulating mitochondrial metabolism.
  • Targeting TSPO may offer a therapeutic strategy for neuroinflammation-related CNS diseases.
Keywords:
TSPOmetabolismmicrogliamitochondrialneuroinflammationphagocytosis

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