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

A Hamasaki, F Sendo, K Nakayama, N Ishida… - The Journal of …, 1998 - rupress.org
A Hamasaki, F Sendo, K Nakayama, N Ishida, I Negishi, K Nakayama, S Hatakeyama
The Journal of experimental medicine, 1998rupress.org
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 …
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 α–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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