Accelerated neutrophil apoptosis in mice lacking A1-a, a subtype of the bcl-2-related A1 gene

Azumi Hamasaki, Fujiro Sendo, Keiko Nakayama, Noriko Ishida, Izumi Negishi, Kei Ichi Nakayama, Shigetsugu Hatakeyama

Research output: Contribution to journalArticlepeer-review

181 Citations (Scopus)

Abstract

To elucidate the role of A1, a new member of the Bcl-2 family of apoptosis regulators active in hematopoietic cell apoptosis, we established mice lacking A1-a, a subtype of the A1 gene in mice (Al-a(-/-) mice). Spontaneous apoptosis of peripheral blood neutrophils of A1-a(-/-) mice was enhanced compared with that of either wild-type mice or heterozygous mutants (A1-a(+/-) mice). Neutrophil apoptosis inhibition induced by lipopolysaccharide treatment in vitro or transendothelial migration in vivo observed in wild-type mice was abolished in both A1-a(-/-) and A1-a(+/-) animals. On the other hand, the extent of tumor necrosis factor α-induced acceleration of neutrophil apoptosis did not differ among A1-a(-/-), A1- a(+/-), and wild-type mice. The descending order oral mRNA expression was wild-type, A1-a(+/-), and A1-a(-/-). Taken together, these results suggest that A1 is involved in inhibition of certain types of neutrophil apoptosis.

Original languageEnglish
Pages (from-to)1985-1992
Number of pages8
JournalJournal of Experimental Medicine
Volume188
Issue number11
DOIs
Publication statusPublished - 1998 Dec 7
Externally publishedYes

Keywords

  • A1
  • Apoptosis
  • Gene disruption
  • Neutrophil
  • bcl-2-related gene

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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