Lee S H, Fujita N, Mashima T, Tsuruo T
Institute of Molecular and Cellular Biosciences, University of Tokyo, Bunkyo-ku, Japan.
Oncogene. 1996 Nov 21;13(10):2131-9.
Mouse malignant T-lymphoma CS-21 cells grow in vitro in the presence of CA-12 lymph node stromal cells, but they undergo apoptotic cell death when separated from CA-12 stromal cells. In the course of examining the nursing effects of CA-12 stromal cells, we found that these cells provided some soluble factors that suppressed CS-21 cell apoptosis. We recently found that cysteine was an antiapoptotic soluble factor. In this report, we identify interleukin-7 (IL-7) as another antiapoptotic soluble factor secreted by CA-12 stromal cells. Although the activity of CPP32-like protease was increased in induction of CS-21 cell apoptosis, the addition of IL-7 suppressed the activity. The expression of Bcl-2 protein was down-regulated when CS-21 cells were cultured alone, but the addition of IL-7 recovered the expression of Bcl-2. These results indicate that CA-12 stromal cells inhibit CS-21 cell apoptosis by producing IL-7, which leads to the suppression of CPP32-like protease activation and the expression of Bcl-2 protein.
小鼠恶性T淋巴瘤CS - 21细胞在CA - 12淋巴结基质细胞存在的情况下可在体外生长,但当与CA - 12基质细胞分离时会发生凋亡性细胞死亡。在研究CA - 12基质细胞的滋养作用过程中,我们发现这些细胞能提供一些可抑制CS - 21细胞凋亡的可溶性因子。我们最近发现半胱氨酸是一种抗凋亡可溶性因子。在本报告中,我们确定白细胞介素 - 7(IL - 7)是CA - 12基质细胞分泌的另一种抗凋亡可溶性因子。虽然在诱导CS - 21细胞凋亡过程中类CPP32蛋白酶的活性增加,但添加IL - 7可抑制该活性。当单独培养CS - 21细胞时,Bcl - 2蛋白的表达下调,但添加IL - 7可恢复Bcl - 2的表达。这些结果表明,CA - 12基质细胞通过产生IL - 7来抑制CS - 21细胞凋亡,这导致类CPP32蛋白酶激活的抑制以及Bcl - 2蛋白的表达。