Kiefer J, Okret S, Jondal M, McConkey D J
Department of Cell Biology, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
J Immunol. 1995 Nov 15;155(10):4525-8.
The involvement of the glucocorticoid receptor (GR) in cAMP-induced apoptosis in a GR-deficient derivative of the CEM.C7 human T-ALL line was investigated. Incubation of the parental CEM.C7 cells with agents that elevate cAMP levels (dibutyryl cAMP and forskolin) resulted in DNA fragmentation characteristic of apoptotic cell death, whereas the GR-deficient ICR.27 cells were insensitive to the cytolytic effects of cAMP. Reconstitution of GR expression by transfection not only restored glucocorticoid sensitivity to the ICR.27 cells, but also promoted sensitivity to induction of apoptosis by cAMP. Thus, cAMP-induced apoptosis in T cells appears to occur via ligand-independent stimulation of at least some aspects of glucocorticoid receptor function.
研究了糖皮质激素受体（GR）在CEM.C7人T-ALL细胞系的GR缺陷衍生物中cAMP诱导的细胞凋亡中的作用。用能提高cAMP水平的试剂（二丁酰cAMP和福斯高林）孵育亲代CEM.C7细胞，导致出现凋亡细胞死亡特征性的DNA片段化，而GR缺陷的ICR.27细胞对cAMP的细胞溶解作用不敏感。通过转染重建GR表达不仅恢复了ICR.27细胞对糖皮质激素的敏感性，还促进了对cAMP诱导凋亡的敏感性。因此，T细胞中cAMP诱导的细胞凋亡似乎是通过对糖皮质激素受体功能至少某些方面的非配体依赖性刺激而发生的。
