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Evidence for apoptotic cell death in the choroid plexus following focal cerebral ischemia
F Gillardon1, C Lenz, W Kuschinsky
1II. Physiologisches Institut der Universität Heidelberg, Germany.
Abstract:
Focal cerebral ischemia in rats subjected to middle cerebral artery (MCA) occlusion results in apoptotic DNA fragmentation and activation of putative cell death effector genes in neurons and functional impairment of the plexus choroideus. In the present study we investigated whether cerebral ischemia may induce apoptotic cell death in the choroid plexus. Using in situ end-labeling by terminal transferase and fluorescein-dUTP, nuclear DNA breaks were detected in the choroid plexus of the lateral ventricle of the ischemic hemisphere after 6 h but not after 1.5 h of MCA occlusion. Intense cytoplasmic immunostaining for pro-apoptotic Bax protein and moderate immunolabeling for Bcl-X was observed in the epithelium of the choroid plexus of the lateral and third ventricles. However, constitutive expression of Bax and Bcl-X proteins in the plexus choroideus did not change significantly following focal ischemia. Thus, cells of the choroid plexus may die by apoptosis after several hours of cerebral ischemia. Modulation of cell death effector genes of the bcl-2 family however, may not be required for apoptotic cell death to occur.
Insights
Cerebral ischemia induces apoptotic cell death in rat choroid plexus after 6 hours of middle cerebral artery occlusion. This cell death occurs without significant changes in pro-apoptotic Bax or Bcl-X protein expression.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Focal cerebral ischemia, induced by middle cerebral artery (MCA) occlusion in rats, leads to neuronal apoptosis and functional impairment.
- The choroid plexus, responsible for cerebrospinal fluid production, may also be affected by ischemic events.
Purpose of the Study:
- To investigate whether cerebral ischemia induces apoptotic cell death in the choroid plexus.
- To examine the role of pro-apoptotic proteins Bax and Bcl-X in this process.
Main Methods:
- Induction of focal cerebral ischemia via middle cerebral artery (MCA) occlusion in rats.
- Detection of nuclear DNA breaks in the choroid plexus using in situ end-labeling (TUNEL assay).
- Immunohistochemical analysis of Bax and Bcl-X protein expression in the choroid plexus epithelium.
Main Results:
- Nuclear DNA breaks, indicative of apoptosis, were detected in the choroid plexus after 6 hours of MCA occlusion, but not after 1.5 hours.
- Intense cytoplasmic immunostaining for Bax and moderate immunolabeling for Bcl-X were observed.
- Constitutive expression levels of Bax and Bcl-X proteins did not significantly change following focal ischemia.
Conclusions:
- Cells of the choroid plexus can undergo apoptosis several hours after focal cerebral ischemia.
- The apoptotic cell death in the choroid plexus following ischemia may not require modulation of bcl-2 family effector genes.