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

Koko Urase, Takashi Momoi, Eriko Fujita, Kyoko Isahara, Yasuo Uchiyama, Akinori Tokunaga, Keiichi Nakayama, Noboru Motoyama

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Caspases and Bcl-xL, the mammalian homologues of the Caenorhabditis elegans (C. elegans) ced-3 and ced-9 genes, respectively, regulate apoptosis of various cells. Caspase-3 is processed into an active form (p20 or p17 and p12) during apoptosis. We investigated the relation between caspase-3 and Bcl-xL during development by examining activation of caspase-3 and apoptotic cells in Bcl-x-deficient (bcl-x(-/-)) mice at embryonic (E) day 11.5. We used a double-staining technique with a cleavage site-directed antibody against caspase-3 (anti-p20/17) and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Bcl-xL-deficiency increased both numbers of p20/17-positive and -negative apoptotic cells in dorsal root ganglia (DRG); the numbers of p20/17-positive apoptotic cells in the caudal parts of the ventral hindbrain and ventral spinal cord; and the numbers of p20/17-negative apoptotic cells in the dorsal midbrain, dorsal hindbrain, and dorsal spinal cord. Thus, Bcl-xL blocks the caspase-3-dependent apoptotic pathway in the restricted regions of the nervous system during development. Furthermore, these observations suggest that Bcl-xL protects against activation of the caspase-3-independent apoptotic pathway. Other caspases or apoptotic mechanisms may also be activated in the nervous systems of bcl-x(-/-) mice. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)69-78
Number of pages10
JournalDevelopmental Brain Research
Volume116
Issue number1
DOIs
Publication statusPublished - Aug 5 1999

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Caspase 3
Neurons
Rhombencephalon
Caspases
Nervous System
Spinal Cord
Apoptosis
Caenorhabditis elegans
In Situ Nick-End Labeling
Spinal Ganglia
Mesencephalon
Staining and Labeling
Antibodies
Genes

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience
  • Developmental Biology

Cite this

Urase, K., Momoi, T., Fujita, E., Isahara, K., Uchiyama, Y., Tokunaga, A., ... Motoyama, N. (1999). Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development. Developmental Brain Research, 116(1), 69-78. https://doi.org/10.1016/S0165-3806(99)00076-0

Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development. / Urase, Koko; Momoi, Takashi; Fujita, Eriko; Isahara, Kyoko; Uchiyama, Yasuo; Tokunaga, Akinori; Nakayama, Keiichi; Motoyama, Noboru.

In: Developmental Brain Research, Vol. 116, No. 1, 05.08.1999, p. 69-78.

Research output: Contribution to journalArticle

Urase, K, Momoi, T, Fujita, E, Isahara, K, Uchiyama, Y, Tokunaga, A, Nakayama, K & Motoyama, N 1999, 'Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development', Developmental Brain Research, vol. 116, no. 1, pp. 69-78. https://doi.org/10.1016/S0165-3806(99)00076-0
Urase, Koko ; Momoi, Takashi ; Fujita, Eriko ; Isahara, Kyoko ; Uchiyama, Yasuo ; Tokunaga, Akinori ; Nakayama, Keiichi ; Motoyama, Noboru. / Bcl-xL is a negative regulator of caspase-3 activation in immature neurons during development. In: Developmental Brain Research. 1999 ; Vol. 116, No. 1. pp. 69-78.
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