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Erschienen in: Clinical Rheumatology 4/2019

19.11.2018 | Original Article

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

Erschienen in: Clinical Rheumatology | Ausgabe 4/2019

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Abstract

Objectives

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.

Method

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.

Results

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).

Conclusions

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.
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Metadaten
Titel
The potential role of Ets-1 and miR-326 in CD19+B cells in the pathogenesis of patients with systemic lupus erythematosus
Publikationsdatum
19.11.2018
Erschienen in
Clinical Rheumatology / Ausgabe 4/2019
Print ISSN: 0770-3198
Elektronische ISSN: 1434-9949
DOI
https://doi.org/10.1007/s10067-018-4371-0

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