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Anisomycin prevents OGD-induced necroptosis by regulating the E3 ligase CHIP

Mi-Bo Tang1,2, Yu-Sheng Li1, Shao-Hua Li1,2

  • 1Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450000, Henan, China.

Scientific Reports
|April 25, 2018
PubMed

Insights

Anisomycin treatment reduces necroptosis, a cell death process in brain injury, by increasing CHIP protein. This finding offers a new therapeutic target for cerebral ischemia.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Necroptosis is a key process in brain injuries like cerebral ischemia.
  • Targeting necroptosis offers a potential therapeutic strategy to prevent cell death.

Purpose of the Study:

  • To investigate the effect of anisomycin on necroptosis in in vitro models of cerebral ischemia.
  • To elucidate the role of carboxyl terminus of Hsc70-interacting protein (CHIP) in anisomycin-mediated attenuation of necroptosis.

Main Methods:

  • Utilized two in vitro models of cerebral ischemia.
  • Administered anisomycin, a protein synthesis inhibitor and c-Jun N-terminal kinase activator.
  • Assessed protein levels of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3).
  • Investigated the necessity of CHIP's co-chaperone and ubiquitin E3 ligase functions.

Main Results:

  • Anisomycin attenuated necroptosis in both cerebral ischemia models.
  • Anisomycin upregulated CHIP expression, leading to reduced RIPK1 and RIPK3 protein levels.
  • CHIP's ability to reduce necroptosis was independent of its co-chaperone and ubiquitin E3 ligase functions.

Conclusions:

  • Activating CHIP expression represents a novel strategy to prevent necroptosis in cerebral ischemia.
  • CHIP modulation offers a potential therapeutic target for treating cerebral ischemia-related diseases.

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