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Abstracts
260 MiR-326 promotes renal injury in murine lupus nephritis
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  1. Yuan Xia1,
  2. Xuan Fang1,
  3. Nan Xiang1,
  4. Xiaojuan Dai1,
  5. Li Jin1,
  6. Xiaomei Li1,
  7. Jinhui Tao1 and
  8. Xiangpei Li2
  1. 1Department of Rheumatology and Immunology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui
  2. 2Department of Rheumatology and Immunology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei

Abstract

Background MicroRNAs play vital role in the immunopathogenesis of human and experimental lupus nephritis, but the contributions of miR-326 to renal injury in systemic lupus erythematosus (SLE) remain to be demonstrated. Here we characterize the function of the miR-326 in MRL/lpr mice of lupus nephritis.

Methods We generated MRL/lpr mice overexpression or silence in miR-326 and analyzed the clinical course of the nephritis with respect to albuminuria. In addition, renal Th17/Treg cells and IL-17A/TGF- expression were detected by flow cytometry and immune-histochemistry respectively.

Results miR-326 overexpression did increase the development of albuminuria in MRL/lpr mice. In contrast, miR-326 silence decreased the development of albuminuria. The characterization of renal CD4 +T cells in miR-326 overexpression mice revealed high numbers of infiltrating Th17 cells and low numbers of infiltrating Tregs. IL-17A and TGF- expression respectively increased and decreased in miR-326 overexpression mice.

Conclusions miR-326 overexpression plays major role in the immunopathogenesis of lupus nephritis in MRL/lpr mice. Thus, our results suggest that miR-326 may be an intriguing new therapeutic approach for patients with lupus nephritis.

Funding Source(s): the National Natural Science Foundation of China 81373186

https://doi.org/10.1136/lupus-2019-lsm.260

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