Cerezo A, Martínez-A C, González A, Gómez J, Rebollo A
Department of Immunology and Oncology, Centro Nacional de Biotecnología, Universidad Autónoma, Campus de Cantoblanco, E-28049 Madrid, Spain.
Cell Death Differ. 1999 Jan;6(1):87-94. doi: 10.1038/sj.cdd.4400458.
A variety of environmental stresses, as well as inflammatory cytokines, induce activation of c-Jun N-terminal kinases. We describe here that IL-2 deprivation-induced apoptosis in TS1alphabeta cells does not modify c-Jun protein levels and correlates Bcl-2 downregulation and an increase in JNK1, but not JNK2, activity directly related to the induction of apoptosis. Indeed, downregulation of JNK1 expression using antisense oligonucleotides inhibits apoptosis induced by IL-2 withdrawal. Overexpression of Bcl-2 promotes cell survival and blocks JNK1 activation as well as apoptosis caused by IL-2 deprivation. This suggests that inhibition of the JNK1 signaling pathway may be a mechanism through which Bcl-2 promotes cell survival and prevents apoptosis triggered by growth factor withdrawal.
多种环境应激以及炎性细胞因子可诱导c-Jun氨基末端激酶激活。我们在此描述，TS1αβ细胞中白细胞介素-2剥夺诱导的凋亡不会改变c-Jun蛋白水平，且与Bcl-2下调以及JNK1（而非JNK2）活性增加相关，而JNK1活性增加与凋亡诱导直接相关。实际上，使用反义寡核苷酸下调JNK1表达可抑制白细胞介素-2撤除诱导的凋亡。Bcl-2过表达可促进细胞存活，并阻断JNK1激活以及白细胞介素-2剥夺引起的凋亡。这表明抑制JNK1信号通路可能是Bcl-2促进细胞存活并防止生长因子撤除触发凋亡的一种机制。
