The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/12/1985/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 11, December 7, 1998 1985-1992

Articles

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

Azumi Hamasaki*, Fujiro Sendo*, Keiko Nakayama{ddagger},§, Noriko Ishida{ddagger}, Izumi Negishi||, Kei-ichi Nakayama{ddagger}, and Shigetsugu Hatakeyama{ddagger}

From the * Department of Immunology and Parasitology, Yamagata University School of Medicine, Yamagata 990-9585, Japan; the {ddagger} 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 in mice (A1-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 {alpha}–induced acceleration of neutrophil apoptosis did not differ among A1-a–/–, A1-a+/–, and wild-type mice. The descending order of A1 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.

Key Words: neutrophil • apoptosis • A1 • bcl-2–related gene • gene disruption

Address correspondence to Fujiro Sendo, Department of Immunology and Parasitology, Yamagata University School of Medicine, 2-2-2 Iida Nishi, Yamagata 990-9585, Japan. Phone: 81-23-628-5263; Fax: 81-23-628-5267; E-mail: fsendo{at}med.id.yamagata-u.ac.jp

This work was partially supported by a Grant-in-Aid for Scientific Research (09470069) from the Ministry of Education, Science, and Culture, Japan.

1 Abbreviations used in this paper: ES, embryonic stem cells; PBN, peripheral blood neutrophils; PEN, peritoneal exudate neutrophils.


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