Kondo E, Yoshino T, Nomura S, Nakamura S, Takahashi K, Teramoto N, Hayashi K, Akagi T
Department of Pathology, Okayama University School of Medicine.
Jpn J Cancer Res. 1994 Mar;85(3):260-5. doi: 10.1111/j.1349-7006.1994.tb02091.x.
Expression of the bcl-2 protein and bcl-2 mRNA at the individual cell level was semiquantitatively examined in normal quiescent peripheral blood lymphocytes and pokeweed mitogen- or concanavalin A and interleukin-2-induced lymphoblasts in vitro by microscopic fluorometry using immunofluorescence and fluorescein-labeled in situ hybridization. Approximately 90% of normal quiescent T and B lymphocytes expressed bcl-2 protein at a level which was compatible with that of bcl-2 mRNA. On the contrary, most mitogen-induced lymphoblasts showed a posttranscriptional suppression of bcl-2 protein expression. However, bcl-2 protein was not downregulated by the posttranscriptional suppression in all lymphocytes activated in vitro, but approximately 15% of the lymphoblasts still expressed bcl-2 protein at a higher level than nontransformed quiescent small lymphocytes; thus bcl-2 protein expression in lymphoblasts showed a distinct bimodal pattern. Furthermore, it was supposed that lymphoblasts with no detectable bcl-2 protein might fall into apoptosis but the remainder, expressing high levels of bcl-2 protein, could escape apoptosis. Thus, the bcl-2 gene may play an important role as a regulator of apoptosis in the human immune system.
通过免疫荧光和荧光素标记原位杂交的显微荧光测定法，在体外对正常静止外周血淋巴细胞以及商陆有丝分裂原或伴刀豆球蛋白A和白细胞介素-2诱导的淋巴母细胞进行个体细胞水平的bcl-2蛋白和bcl-2 mRNA表达的半定量检测。约90%的正常静止T和B淋巴细胞表达的bcl-2蛋白水平与bcl-2 mRNA水平相符。相反，大多数有丝分裂原诱导的淋巴母细胞显示出bcl-2蛋白表达的转录后抑制。然而，在所有体外激活的淋巴细胞中，bcl-2蛋白并未因转录后抑制而下调，约15%的淋巴母细胞仍表达比未转化的静止小淋巴细胞更高水平的bcl-2蛋白；因此，淋巴母细胞中bcl-2蛋白表达呈现出明显的双峰模式。此外，推测未检测到bcl-2蛋白的淋巴母细胞可能会发生凋亡，而其余表达高水平bcl-2蛋白的细胞可以逃避凋亡。因此，bcl-2基因可能作为人类免疫系统中凋亡的调节因子发挥重要作用。
