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Hsa_circ_0010957 水平在系统性红斑狼疮患者的 CD4 T 细胞中升高并海绵 microRNA-125b。

Hsa_circ_0010957 level is increased and sponges microRNA‑125b in CD4 T cells of patients with systemic lupus erythematosus.

机构信息

Department of Rheumatology and Immunology, Jinhua Municipal Central Hospital, Jinhua Hospital of Zhejiang University, Jinhua, Zhejiang 321000, P.R. China.

Department of Joint Surgery, Jinhua Municipal Central Hospital, Jinhua Hospital of Zhejiang University, Jinhua, Zhejiang 321000, P.R. China.

出版信息

Mol Med Rep. 2021 Jun;23(6). doi: 10.3892/mmr.2021.12108. Epub 2021 Apr 21.

DOI:10.3892/mmr.2021.12108
PMID:33880592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8097751/
Abstract

Systemic lupus erythematosus (SLE) is a severe autoimmune disorder, the pathogenesis of which remains largely unknown. The present study aimed to investigate the role and mechanism of circular RNAs in the etiopathogenesis of SLE. CD4 T cells in patients with SLE expressed higher levels of hsa_circ_0010957 compared with healthy individuals and was a good differentiator of the active from inactive SLE disease. It was also determined that hsa_circ_0010957 mediated microRNA (miR)‑125b/STAT3 signaling and subsequent secretion of inflammatory cytokines interleukin (IL)‑18, IL‑6 and IL‑17, which are important factors in the process of SLE. Hsa_circ_0010957 abrogated the proinflammatory effect of IL‑6 via the blockade of STAT3 signaling. In conclusion, increased hsa_circ_0010957 may be involved in SLE pathogenesis via miR‑125b/STAT3 signaling. Hsa_circ_0010957 promises to be a potential biomarker and therapeutic target for SLE.

摘要

系统性红斑狼疮(SLE)是一种严重的自身免疫性疾病,其发病机制在很大程度上尚不清楚。本研究旨在探讨环状 RNA 在 SLE 发病机制中的作用和机制。与健康个体相比,SLE 患者的 CD4 T 细胞表达更高水平的 hsa_circ_0010957,并且是区分 SLE 疾病活动与非活动的良好指标。还确定 hsa_circ_0010957 介导 microRNA(miR)-125b/STAT3 信号转导以及随后的炎症细胞因子白细胞介素(IL)-18、IL-6 和 IL-17 的分泌,这些都是 SLE 过程中的重要因素。hsa_circ_0010957 通过阻断 STAT3 信号转导来消除 IL-6 的促炎作用。总之,hsa_circ_0010957 的增加可能通过 miR-125b/STAT3 信号转导参与 SLE 的发病机制。hsa_circ_0010957 有望成为 SLE 的潜在生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/e1c25ebceb8e/mmr-23-06-12108-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/4b3585d6ce3a/mmr-23-06-12108-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/e7854bc0613d/mmr-23-06-12108-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/a32bb871e71a/mmr-23-06-12108-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/d06273269d27/mmr-23-06-12108-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/5a8525d68d0c/mmr-23-06-12108-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/e1c25ebceb8e/mmr-23-06-12108-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/4b3585d6ce3a/mmr-23-06-12108-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/e7854bc0613d/mmr-23-06-12108-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/a32bb871e71a/mmr-23-06-12108-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/d06273269d27/mmr-23-06-12108-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/5a8525d68d0c/mmr-23-06-12108-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4057/8097751/e1c25ebceb8e/mmr-23-06-12108-g05.jpg

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