Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development

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Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue
09:17

Ex Utero Electroporation and Organotypic Slice Culture of Mouse Hippocampal Tissue

Published on: March 4, 2015

K Urase1, T Momoi, E Fujita

  • 1Division of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502, Japan.

Brain Research. Developmental Brain Research
|August 14, 1999
PubMed

Insights

Bcl-xL protein regulates apoptosis during development. In mice lacking Bcl-xL, caspase-3 activation and cell death increased in specific nervous system regions, indicating Bcl-xL

Area of Science:

  • Developmental biology
  • Cell biology
  • Neuroscience

Background:

  • Apoptosis, or programmed cell death, is crucial for development.
  • Caspases and Bcl-xL are key regulators of apoptosis.
  • Bcl-xL is the mammalian homologue of C. elegans ced-9, while caspases are homologues of ced-3.

Purpose of the Study:

  • To investigate the relationship between caspase-3 activation and Bcl-xL during embryonic development.
  • To examine the role of Bcl-xL in regulating apoptosis in the developing nervous system.

Main Methods:

  • Utilized Bcl-x-deficient (bcl-x(-/-)) mice at embryonic day 11.5.
  • Employed a double-staining technique combining a caspase-3 cleavage site-directed antibody (anti-p20/17) and TUNEL assay.
  • Quantified apoptotic cells and caspase-3 activation in various neural tissues.

Main Results:

  • Bcl-xL deficiency led to increased numbers of both caspase-3-positive and -negative apoptotic cells in dorsal root ganglia (DRG).
  • Increased caspase-3-positive apoptotic cells were observed in the caudal ventral hindbrain and ventral spinal cord.
  • Increased caspase-3-negative apoptotic cells were found in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord.

Conclusions:

  • Bcl-xL inhibits the caspase-3-dependent apoptotic pathway in specific regions of the developing nervous system.
  • Bcl-xL may also protect against caspase-3-independent apoptotic pathways.
  • Alternative caspases or apoptotic mechanisms might be activated in Bcl-xL-deficient mouse nervous systems.

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