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, Kei Ichi Nakayama, Noboru Motoyama

研究成果: Contribution to journalArticle査読

18 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)69-78
ページ数10
ジャーナルDevelopmental Brain Research
116
1
DOI
出版ステータス出版済み - 8 5 1999

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience
  • Developmental Biology

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