Gottschalk A R, Joseph L J, Quintáns J
Department of Pathology, University of Chicago, IL 60637.
Eur J Immunol. 1993 Aug;23(8):2011-5. doi: 10.1002/eji.1830230843.
To determine whether the absence of inducible Egr-1 expression correlates with apoptosis and growth arrest, we compared the inducible expression of two Egr family members (Egr-1 and Egr-2) in three sublines of WEHI-231. Expression of Egr-2 is induced in all sublines of WEHI-231 following surface immunoglobulin (sIg) cross-linking, but Egr-1 expression is induced in only two. We find that the lack of inducible Egr-1 expression corresponded to an increase in the methylation pattern of the Egr-1 gene. In spite of these differences in Egr-1 expression, all the sublines demonstrate similar inhibition of [3H] thymidine incorporation following anti-Ig treatment. Growth arrest leads to apoptosis in only two of the sublines, but apoptosis does not correlate with the absence of inducible Egr-1 expression. Demethylation, by treatment with 5-azacytidine, in the Egr-1 non-expressing subline allows for induction of Egr-1 expression by anti-Ig, but fails to prevent growth arrest and apoptosis. Therefore, we conclude that the lack of Egr-1 expression is not responsible for either the apoptotic response or growth arrest induced by anti-Ig in WEHI-231.
为了确定诱导型Egr-1表达的缺失是否与细胞凋亡和生长停滞相关,我们比较了WEHI-231三个亚系中两种Egr家族成员(Egr-1和Egr-2)的诱导型表达。在表面免疫球蛋白(sIg)交联后,WEHI-231的所有亚系中均诱导了Egr-2的表达,但只有两个亚系诱导了Egr-1的表达。我们发现,诱导型Egr-1表达的缺失与Egr-1基因甲基化模式的增加相对应。尽管Egr-1表达存在这些差异,但所有亚系在抗Ig处理后均表现出对[3H]胸苷掺入的类似抑制。生长停滞仅在两个亚系中导致细胞凋亡,但细胞凋亡与诱导型Egr-1表达的缺失无关。通过用5-氮杂胞苷处理使Egr-1不表达的亚系去甲基化,可使抗Ig诱导Egr-1表达,但不能阻止生长停滞和细胞凋亡。因此,我们得出结论,Egr-1表达的缺失不是抗Ig在WEHI-231中诱导的细胞凋亡反应或生长停滞的原因。