单位：[1]Institute of Dermatology and Department of Dermatology, the First Affiliated Hospital, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui 230032, China[2]Key Laboratory of Dermatology, Anhui Medical University, Ministry of Education, Hefei, Anhui 230032, China[3]Department of Dermatology, China–Japan Friendship Hospital, East Street Cherry Park, Chaoyang District, Beijing 100029, China
Objective: This study was aimed to explore the effect of Bach2 on B cells in systemic lupus erythematosus (SLE), as well as the underlying mechanisms. Methods: Expression of Bach2, phosphorylated-Bach2 (p-Bach2), Akt, p-Akt and BCR-ABL (p210) in B cells isolated from SLE patients and the healthy persons were assessed by Western blot. Immunofluorescence staining was performed to assess the localization of Bach2 in B cells. Enzyme-linked immunosorbent assay (ELISA) was employed to detect IgG produced by B cells. Cell counting kit-8 (CCK-8) and Annexin-V FITC/PI double staining assay were adopted to evaluate cell proliferation and apoptosis in B cells, respectively. Results: Compared to the healthy controls, Bach2, p-Akt and p210 were significantly decreased, while nuclear translocation of Bach2, IgG, CD40 and CD86 obviously up-regulated in B cells from SLE patients. Bach2 significantly inhibited the proliferation, promoted apoptosis of B cells from SLE patients, whereas BCR-ABL dramatically reversed cell changes induced by Bach2. Besides, BCR-ABL also inhibited nuclear translocation of Bach2 in B cells from SLE patients. Further, LY294002 treatment had no effect on decreased expression of Bach2 induced by BCR-ABL, but significantly eliminated BCR-ABL-induced phosphorylation of Bach2 and restored reduced nuclear translocation of Bach2 induced by BCR-ABL in B cells from SLE. Conclusions: Bach2 may play a suppressive role in B cells from SLE, and BCR-ABL may inhibit the nuclear translocation of Bach2 via serine phosphorylation through the PI3K pathway.
基金：
National Key Research and Development [2017YFC0909001]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81402590, 81371722]; National Key Basic Research Program of ChinaNational Basic Research Program of China [2014CB541901]; Research Project of the Chinese Ministry of EducationMinistry of Education, China [213018A]
第一作者单位：[1]Institute of Dermatology and Department of Dermatology, the First Affiliated Hospital, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui 230032, China[2]Key Laboratory of Dermatology, Anhui Medical University, Ministry of Education, Hefei, Anhui 230032, China
通讯作者：
通讯机构：[1]Institute of Dermatology and Department of Dermatology, the First Affiliated Hospital, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui 230032, China[2]Key Laboratory of Dermatology, Anhui Medical University, Ministry of Education, Hefei, Anhui 230032, China[*1]Institute of Dermatology and Department of Dermatology, the First Affiliated Hospital, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui 230032, China
推荐引用方式(GB/T 7714)：
Zhu Zhengwei,Yang Chao,Wen Leilei,et al.Bach2 regulates aberrant activation of B cell in systemic lupus erythematosus and can be negatively regulated by BCR-ABL/PI3K[J].EXPERIMENTAL CELL RESEARCH.2018,365(1):138-144.doi:10.1016/j.yexcr.2018.02.034.
APA：
Zhu, Zhengwei,Yang, Chao,Wen, Leilei,Liu, Lu,Zuo, Xianbo...&Sheng, Yujun.(2018).Bach2 regulates aberrant activation of B cell in systemic lupus erythematosus and can be negatively regulated by BCR-ABL/PI3K.EXPERIMENTAL CELL RESEARCH,365,(1)
MLA：
Zhu, Zhengwei,et al."Bach2 regulates aberrant activation of B cell in systemic lupus erythematosus and can be negatively regulated by BCR-ABL/PI3K".EXPERIMENTAL CELL RESEARCH 365..1(2018):138-144
