Evidence map›Paper›PMID 32467986›Full record

ArticleMolecular medicine reports2020

Downregulated miR‑29a promotes B cell overactivation by upregulating Crk‑like protein in systemic lupus erythematosus.

Xinyu Shi, Lulu Ye, Shuqi Xu, Gangqiang Guo, Ziyi Zuo, Mengke Ye, Lejiang Zhu, Baoqing Li, Xiangyang Xue, Qiaoai Lin and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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  16. Epigenetic Regulations of AhR in the Aspect of Immunomodulation.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Xinyu Shi *Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Lulu Ye *Department of Laboratory Medicine, Anqing Petrochemical Hospital, Anqing, Anhui 246000, P.R. China.
Shuqi Xu *First Clinical College, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Gangqiang GuoDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Ziyi ZuoFirst Clinical College, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Mengke YeFirst Clinical College, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Lejiang ZhuDepartment of Nephrology, Wenzhou Central Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Baoqing LiDepartment of Laboratory Medicine, Second Affiliated Hospital & Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Xiangyang XueDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Qiaoai LinDepartment of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Xiaokai DingDepartment of Nephrology, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Wenzhou Medical University · CNAnqing City Hospital · CNFirst Affiliated Hospital of Wenzhou Medical University · CNSecond Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disorder; however, the pathogenesis is not fully understood. Accumulating evidence suggested an important role of microRNAs (miRNA/miR) in autoimmunity. The present study aimed therefore to determine the miRNA expression patterns in the B cells from the peripheral blood of 66 patients with SLE and 10 healthy controls (HCs) by using an Affymetrix GeneChip® miRNA 2.0 array. In addition, next‑generation sequencing was used to obtain the peripheral blood mononuclear cell (PBMC) miRNA profiles from three patients with SLE and three HCs. Candidate miRNAs that were considered to contribute to the pathogenesis of SLE were obtained based on the intersection of miRNA profiles. The analysis revealed a significant downregulation in miR‑29a expression levels in B cells from patients with SLE, which was subsequently verified using reverse transcription‑quantitative PCR. Based on these results, the expression pattern of miR‑29a in SLE was further investigated and its role in the hyperactivity of B cells was determined. miR‑29a inhibitors and mimics were transfected into PBMCs obtained from HCs and patients with SLE, and an ELISA was used to demonstrate that miR‑29a inhibition increased the production of IgG. Bioinformatics analysis predicted Crk‑like protein (CRKL) as a target gene of miR‑29a in patients with SLE. Therefore, CRKL expression levels were compared between patients with SLE and HCs by using western blotting, and its direct transcriptional regulation by miR‑29a was determined using a dual‑luciferase reporter assay. Low expression levels of miR‑29a were revealed to upregulate the expression levels of CRKL in B cells, and the protein expression levels of CRKL in patients with SLE were significantly upregulated compared with the HCs. In conclusion, the results from the present study suggested that miR‑29a may affect IgG antibody secretion in B cells by regulating CRKL, thereby contributing to the development and progression of SLE, which offers a novel candidate target for treatment.

Indexed as

Adaptor Proteins, Signal TransducingAdultB-LymphocytesCell LineComputational BiologyDown-RegulationFemaleGene Expression ProfilingGene Expression RegulationHigh-Throughput Nucleotide SequencingHumansImmunoglobulin GLeukocytes, MononuclearLupus Erythematosus, SystemicMaleMicroRNAsAdaptor Proteins, Signal TransducingImmunoglobulin GMicroRNAsMIRN29a microRNA, humanB cellcrk-like proteinigG antibodymicrorna-29asystemic lupus erythematosus

Identifiers

PMID32467986
PMCPMC7339478
OpenAlexW3028277002

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.