Yan Y, Wang S, Lin C
State Key Laboratory for Organ Failure Research & National Clinical Research Center for Kidney Disease, Guangdong Provincial Clinical Research Center for Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Affiliated Maternity and Child Health Hospital of Anhui Medical University, Maternity and Child Health Hospital of Anhui Province, Hefei, China.
Bull Exp Biol Med. 2022 Dec;174(2):259-264. doi: 10.1007/s10517-023-05685-6. Epub 2023 Jan 5.
We explored the potential link between RelA and BCL11B transcription factors. To this end, Jurkat and Raji cells (Jurkat:Raji 10:1), as well as normal human peripheral blood T cells, were activated by staphylococcal enterotoxin A (SEA) and the expressions of both BCL11B and RelA mRNA and proteins were detected. BCL11B small interfering RNA was then transduced into Jurkat cells. Under the effect of SEA stimulation, the expression of BCL11B and RelA mRNA increased in two types of T cell lines over time, and the results were comparable with the levels of expression of BCL11B and RelA proteins. In the BCL11B-knockdown cells, the expression of RelA protein did not increase. These findings suggest that BCL11B regulates RelA expression in Jurkat cells and human peripheral blood T cells from healthy donors via the T-cell receptor signaling pathway.
我们探究了RelA与BCL11B转录因子之间的潜在联系。为此,用金黄色葡萄球菌肠毒素A(SEA)激活Jurkat细胞和Raji细胞(Jurkat:Raji为10:1)以及正常人外周血T细胞,并检测BCL11B和RelA的mRNA及蛋白表达。随后将BCL11B小干扰RNA转导至Jurkat细胞中。在SEA刺激作用下,两种T细胞系中BCL11B和RelA的mRNA表达随时间增加,结果与BCL11B和RelA蛋白的表达水平相当。在BCL11B敲低的细胞中,RelA蛋白表达未增加。这些发现表明,BCL11B通过T细胞受体信号通路调节Jurkat细胞和健康供体人外周血T细胞中RelA的表达。