Lymphoma cells protected from apoptosis by dysregulated bcl-2 continue to bind Annexin V in response to B-cell receptor engagement:: A cautionary tale
Lymphoma cells protected from apoptosis by dysregulated bcl-2 continue to bind Annexin V in response to B-cell receptor engagement:: A cautionary tale
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DOI：
10.1016/j.leukres.2005.05.018
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发表时间：
2006-01-01
影响因子：
2.7
通讯作者：
Gordon, J
中科院分区：
文献类型：
--
作者：
Holder, MJ;Barnes, NM;Gordon, J
磷脂酰丝氨酸（PS）从表面膜脂质双层的内小叶到外小叶的易位是细胞进入凋亡程序的特征性早期事件，通常通过膜联蛋白V（AV）的Ca 2+依赖性结合来评估。在这里，我们表明，淋巴瘤细胞保护凋亡的表达bcl-2转基因或凭借t（14;18）（q32;q21）易位继续注册增强AV结合BCR交联。诱导的AV结合出现BCR选择性，因为它没有在Bcl-2（高）细胞中进行响应钙离子载体或抗抑郁药氟西汀，其中每一个激活Bcl-2（低）当量的完整凋亡程序。AV阳性细胞在交联BCR共受体CD 19时确实增加，尽管它是完全非凋亡信号。这些发现提示在解释将膜联蛋白V结合作为淋巴瘤B细胞凋亡的唯一或主要指标的研究时应谨慎。(c)2005爱思唯尔有限公司保留所有权利。
Translocation of phosphatidylserine (PS) from the inner to outer leaflet of the surface membrane lipid bilayer, a characteristic early event of cells entering the apoptotic program, is routinely assessed by the Ca2+ -dependent binding of Annexin V (AV). Here, we show that lymphoma cells protected from apoptosis by expression of a bcl-2 transgene or by virtue of the t(14;18)(q32;q21) translocation continue to register enhanced AV binding in response to BCR crosslinking. Induced AV binding appeared BCR-selective in that it did not proceed in Bcl-2(high) cells in response to calcium ionophore or the antidepressant fluoxetine, each of which activate the full apoptotic program in Bcl-2(low) equivalents. AV-positive cells did increase on crosslinking the BCR co-receptor CD19, despite it being a completely non-apoptotic signal. These findings advise caution when interpreting studies where Annexin V binding is used as a sole, or major, indicator of apoptotic death among lymphoma B cells. (c) 2005 Elsevier Ltd. All rights reserved.