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缺乏bcl-2相关A1基因的A1-a亚型的小鼠中嗜中性粒细胞凋亡加速。

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

作者信息

Hamasaki A, Sendo F, Nakayama K, Ishida N, Negishi I, Nakayama K, Hatakeyama S

机构信息

Department of Immunology and Parasitology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.

出版信息

J Exp Med. 1998 Dec 7;188(11):1985-92. doi: 10.1084/jem.188.11.1985.

DOI:10.1084/jem.188.11.1985
PMID:9841913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2212378/
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.

摘要

为阐明凋亡调节因子Bcl-2家族的新成员A1在造血细胞凋亡中的作用，我们构建了缺失小鼠A1基因的一个亚型A1-a的小鼠（A1-a-/-小鼠）。与野生型小鼠或杂合突变体（A1-a+/-小鼠）相比，A1-a-/-小鼠外周血中性粒细胞的自发凋亡增强。在野生型小鼠中观察到的体外脂多糖处理诱导的中性粒细胞凋亡抑制或体内跨内皮迁移，在A1-a-/-和A1-a+/-动物中均被消除。另一方面，肿瘤坏死因子α诱导的中性粒细胞凋亡加速程度在A1-a-/-、A1-a+/-和野生型小鼠之间没有差异。A1 mRNA表达的降序排列为野生型、A1-a+/-和A1-a-/-。综上所述，这些结果表明A1参与了对某些类型中性粒细胞凋亡的抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/d9123e043e65/JEM980425.f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/6e36da08f90d/JEM980425.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/fdbdeb830729/JEM980425.f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/2ac946b0ae03/JEM980425.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/baffb7f0e518/JEM980425.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/d9123e043e65/JEM980425.f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/6e36da08f90d/JEM980425.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/fdbdeb830729/JEM980425.f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/2ac946b0ae03/JEM980425.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/baffb7f0e518/JEM980425.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2984/2212378/d9123e043e65/JEM980425.f5.jpg

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在急性肺炎症和腹膜炎期间，A1 无生存促进作用并不影响炎症细胞的体内存活。
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