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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
11:32

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Function of BID -- a molecule of the bcl-2 family -- in ischemic cell death in the brain

Nikolaus Plesnila1, Sandra Zinkel, Sepideh Amin-Hanjani

  • 1Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA. plesnila@icf.med.uni-muenchen.de

European Surgical Research. Europaische Chirurgische Forschung. Recherches Chirurgicales Europeennes
|February 28, 2002
PubMed

Insights

The proapoptotic molecule BID is expressed in the brain and activated during cerebral ischemia. BID contributes to nerve cell death in stroke by promoting cytochrome c release and caspase activation.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Mitochondrial mechanisms, including cytochrome c release, are implicated in neuronal and glial cell death during cerebral ischemia.
  • The proapoptotic molecule BID, a member of the bcl-2 family, promotes cytochrome c release.

Purpose of the Study:

  • To investigate BID expression and activation in the brain following cerebral ischemia.
  • To determine if BID contributes to ischemic cell death in vivo.

Main Methods:

  • Western blot analysis to detect BID expression in mouse brain and cultured neurons.
  • In vivo middle cerebral artery occlusion model in mice.
  • Assessment of infarct volume and cytochrome c release in BID knockout (BID-/-) mice.

Main Results:

  • BID was detected in the cytosol of mouse brain and primary cultured neurons.
  • Neuronal BID was identified as a substrate for caspase 8.
  • BID cleavage was observed in vivo 4 hours after middle cerebral artery occlusion.
  • BID-/- mice exhibited a 67% reduction in infarction and a 41% decrease in cytochrome c release compared to wild-type mice.

Conclusions:

  • The proapoptotic molecule BID is expressed and activated in the brain during cerebral ischemia.
  • BID contributes to ischemic neuronal death by facilitating cytochrome c release and activating caspase pathways.

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