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

Overview

Journal J Exp Med

Specialties Allergy & Immunology
General Medicine

Date 1998 Dec 8

PMID 9841913

Citations 69

Authors

A Hamasaki

F Sendo

N Ishida

I Negishi

K Nakayama

S Hatakeyama

Affiliations

Soon will be listed here.

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 (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.

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