Accelerated Neutrophil Apoptosis in Mice Lacking A1-a, a Subtype of the bcl-2-related A1 Gene

doi:10.1084/jem.188.11.1985

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J. Exp. Med., Volume 188, Number 11, December 7, 1998 1985-1992

Accelerated Neutrophil Apoptosis in Mice Lacking A1-a, a Subtype of the bcl-2-related A1 Gene

By Azumi Hamasaki,^* Fujiro Sendo,^* Keiko Nakayama,^§ Noriko Ishida, Izumi Negishi, Kei-ichi Nakayama, and Shigetsugu Hatakeyama

From the ^* Department of Immunology and Parasitology, Yamagata University School of Medicine, Yamagata 990-9585, Japan; the Department of Molecular and Cellular Biology and the ^§ Laboratory of Embryonic and Genetic Engineering, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan; and the Department of Dermatology, Gunma University School of Medicine, Maebashi 371-8511, Japan

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 inmice (A1-a^/ mice). Spontaneous apoptosis of peripheral blood neutrophilsof A1-a^/ mice was enhanced compared with that of either wild-type miceor heterozygous mutants (A1-a^+/ mice). Neutrophil apoptosis inhibition induced by lipopolysaccharidetreatment in vitro or transendothelial migration in vivo observedin wild-type mice was abolished in both A1-a^/ and A1-a^+/ animals. On the other hand, the extent of tumor necrosis factor $alpha$ -induced acceleration of neutrophil apoptosis did not differamong A1-a^/, A1-a^+/, and wild-type mice. The descending order of A1 mRNA expressionwas wild-type, A1-a^+/, and A1-a^/. Taken together, these results suggest that A1 is involved ininhibition of certain types of neutrophil apoptosis.

Key words: neutrophil; apoptosis; A1; bcl-2-related gene; gene disruption

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