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Proinflammation effect of Mst1 promotes BV-2 cell death via augmenting Drp1-mediated mitochondrial fragmentation and

Hong Tian1, Kang Wang2, Miao Jin2

  • 1Department of Neurosurgery, China-Japan Friendship Hospital, Beijing, China.

Journal of Cellular Physiology
|July 9, 2019
PubMed

Insights

Mammalian Ste20-like kinase 1 (Mst1) promotes neuroinflammation by activating the JNK-Drp1-mitochondrial fission pathway. Inhibiting Mst1 protects neurons, offering a new therapeutic target for neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Neuroinflammation is increasingly recognized in neurodegenerative diseases.
  • Mammalian Ste20-like kinase 1 (Mst1), a Hippo pathway factor, is linked to cell death, but its role in neuroinflammation is understudied.

Purpose of the Study:

  • To investigate the role of Mst1 in lipopolysaccharide (LPS)-induced neuroinflammation.
  • To elucidate the molecular mechanisms by which Mst1 influences neuronal survival and mitochondrial function.

Main Methods:

  • BV-2 microglial cells were treated with LPS.
  • Mst1 expression and knockdown were analyzed.
  • Mitochondrial fission, Drp1 expression, and JNK signaling pathway activation were assessed.
  • Cell viability and mitochondrial homeostasis were evaluated.

Main Results:

  • LPS treatment upregulated Mst1 expression.
  • Mst1 knockdown enhanced BV-2 cell viability and survival under LPS exposure.
  • Mst1 deletion reduced mitochondrial fission by repressing Drp1 expression.
  • JNK pathway activation reversed the protective effects of Mst1 knockdown on neuronal mitochondria.

Conclusions:

  • Mst1 upregulation and subsequent activation of the JNK-Drp1-mitochondrial fission pathway contribute to neuroinflammation.
  • Modulating the Mst1-JNK-Drp1-mitochondrial fission axis presents a novel therapeutic strategy for neurodegenerative diseases.
Keywords:
Drp1JNKcell deathmitochondrial fissionneuroninflammation

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