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Updated: May 13, 2026
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
MicroRNA-30a promotes B cell hyperactivity in patients with systemic lupus erythematosus by direct interaction with
1Beijing Institute of Basic Medical Sciences, People's Hospital, and Peking University, Beijing, China.
Objective:
To investigate why the level of Lyn is significantly decreased in B cells from a majority of patients with systemic lupus erythematosus (SLE) and to determine the role of microRNA-30a (miR-30a) in SLE B cell hyperactivity.
Methods:
Luciferase reporter gene assays were performed to identify the interaction between miR-30a and the 3'-untranslated region (3'-UTR) of Lyn. Levels of miR-30a in B cells were determined by TaqMan quantitative polymerase chain reaction (qPCR), Lyn messenger RNA levels were tested with real-time qPCR, and protein levels of Lyn were determined using Western blotting. The quantity of IgG was determined by enzyme-linked immunosorbent assay. The proliferation of B cells was measured using (3) H-thymidine incorporation.
Results:
In B cell lines, miR-30a, but not miR-30b, miR-30c, miR-30d, or miR-30e, could specifically bind the 3'-UTR of Lyn, and overexpression of miR-30a inhibited the levels of Lyn. The level of miR-30a in B cells was significantly higher in SLE patients compared to healthy donors. The level of miR-30a was negatively associated with the level of Lyn in B cells. Overexpression of miR-30a was found to promote B cell proliferation and the production of IgG antibodies. The effect of miR-30a could be abrogated by inducing overexpression of Lyn in B cells.
Conclusion:
These results reveal that elevated expression of miR-30a is responsible for the reduction in levels of Lyn in B cells from patients with SLE, suggesting that miR-30a plays an important role in B cell hyperactivity.
