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PDCD4 Simultaneously Promotes Microglia Activation via PDCD4-MAPK-NF-κB Positive Loop and Facilitates Neuron

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Programmed cell death factor 4 (PDCD4) promotes neuroinflammation and neuronal apoptosis in the central nervous system (CNS). Targeting this molecule may offer a new therapeutic strategy for CNS diseases.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Neuroinflammation and neuronal injury are hallmarks of central nervous system (CNS) diseases.
  • Identifying shared regulatory molecules is crucial for developing effective therapeutic targets.
  • The role of Programmed cell death factor 4 (PDCD4) in CNS neuroinflammation is not well understood.

Purpose of the Study:

  • To investigate the expression and function of PDCD4 in the context of CNS neuroinflammation and neuronal injury.
  • To elucidate the molecular mechanisms underlying PDCD4's role in microglial activation and neuronal apoptosis.
  • To explore PDCD4 as a potential therapeutic target for neuroinflammatory diseases.

Main Methods:

  • Utilized a lipopolysaccharide (LPS)-induced neuroinflammation mouse model and in vitro microglial activation models.
  • Employed shRNA to silence PDCD4 expression.
  • Analyzed the phosphorylation of MAPKs (p38, ERK, JNK) and NF-κB p65.
  • Investigated PDCD4's role in H2O2-induced neuronal oxidative damage model.
  • Assessed the expression of pro-apoptotic proteins BAX and Cleaved-PARP.

Main Results:

  • PDCD4 expression was elevated in injured neurons and activated microglia in the inflamed brain.
  • Silencing PDCD4 reduced microglial inflammatory activation by inhibiting MAPK and NF-κB signaling.
  • A positive feedback loop between PDCD4 and MAPK/NF-κB signaling was identified in microglia.
  • PDCD4 knockdown decreased pro-apoptotic protein expression in neurons, indicating its pro-apoptotic role.
  • PDCD4 was found to promote both microglial activation and neuronal apoptosis.

Conclusions:

  • PDCD4 acts as a central regulator in CNS diseases, promoting both microglial inflammatory activation and oxidative stress-induced neuronal apoptosis.
  • The PDCD4-MAPK-NF-κB positive feedback loop in microglia is a key signaling pathway in neuroinflammation.
  • PDCD4 represents a promising therapeutic target for neuroinflammatory diseases.