The potential role of Ets-1 and miR-326 in CD19+B cells in the pathogenesis of patients with systemic lupus erythematosus

• DOI: 10.1007/s10067-018-4371-0
• Publication Date: 2018-11-19T13:58:54Z
• Authors: Li Jin; Xuan Fang; Chao Dai; Nan Xiang; Jinhui Tao; Xiaoge Sun; Farhana Azmi; Qi Cao; Xiaomei Li; Yiping Wang; Xiangpei Li
• Keywords: Adult; Male; B-Lymphocytes; 0303 health sciences; Antigens, CD19; Cell Differentiation; Flow Cytometry; 3. Good health; Proto-Oncogene Protein c-ets-1; MicroRNAs; 03 medical and health sciences; Humans; Lupus Erythematosus, Systemic; Female

The aim of this study was to investigate the B cell-associated transcription factors, Ets-1 and microRNA, miR-326 in systemic lupus erythematosus (SLE) patients, and their correlation with the pathogenesis of SLE.A total of 44 SLE patients and 20 healthy controls were enrolled in this research, all patients fulfilled the American College of Rheumatology classification criteria for SLE. The mRNA expression of Ets-1 and miR-326 in CD19+B cells from SLE patients were examined by qRT-PCR. The percentages of CD19+CD138+plasma cells were analyzed by Flow cytometry.We found decreased expression of Ets-1 mRNA in SLE patients compared with the healthy controls ([0.228 (0.145, 0.507)] vs [0.583 (0.452, 0.763)], p = 0.001),while increased expression of miR-326 mRNA in CD19+B cells SLE patients compared with the healthy controls([1.092 (0.457, 2.855)] vs [0.685 (0.274, 0.819)], p = 0.008). The percentage of CD19+CD138+plasma cells in SLE patients was higher than that of healthy controls (0.55 ± 0.21% vs 0.36 ± 0.21%, p = 0.002). Moreover, a negative correlation between expression of Ets-1 mRNA and miR-326 mRNA in CD19+B cells was detected (r = - 0.334, p = 0.027). A significant association between the occurrences of CD19+CD138+plasma cells and the levels of Ets-1 mRNA and miR-326 mRNA was observed (r = - 0.417, p = 0.005 and r = 0.482, p = 0.001, respectively).Our results suggest that miR-326 might promote B cells differentiation by targeting Ets-1, a negative regulator of B cells differentiation and therefore participate in the pathogenesis of SLE.