Evidence map›Paper›PMID 34431214›Full record

ArticleJournal of cellular and molecular medicine2021

MiR-363-5p modulates regulatory T cells through STAT4-HSPB1-Notch1 axis and is associated with the immunological abnormality in Graves' disease.

Xianlun Yin, Junfeng Ge, Xiurong Ge, Jing Gao, Xinhuan Su, Xiaowei Wang, Qunye Zhang, Zhe Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  3. Article
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

8 authors at 2 institutions in 1 country.

Xianlun YinThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0001-6465-5581
Junfeng GeDepartment of Anesthesiology, Jinan Second People's Hospital, Jinan, Shandong, China.ORCID 0000-0001-8435-0443
Xiurong GeDivision of Endocrinology and Metabolism, Division of Geriatrics, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Shandong Institute of Endocrine and Metabolic Disease, Shandong University, Jinan, China.ORCID 0000-0002-5748-3117
Jing GaoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0002-1462-5365
Xinhuan SuDivision of Endocrinology and Metabolism, Division of Geriatrics, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Shandong Institute of Endocrine and Metabolic Disease, Shandong University, Jinan, China.ORCID 0000-0003-2273-7831
Xiaowei WangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0002-9427-3477
Qunye ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0003-1535-9182
Zhe WangDivision of Endocrinology and Metabolism, Division of Geriatrics, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Shandong Institute of Endocrine and Metabolic Disease, Shandong University, Jinan, China.ORCID 0000-0003-4036-7969
Shandong University · CNXian Yang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiRNAs are a class of small non-coding RNAs with ability to regulate function of Treg cells and are involved in many autoimmune diseases. Our previous study found that miR-363-5p expression was significantly upregulated in peripheral Treg cells of GD patients. Herein, we aimed to investigate its effect and mechanism on Treg cell dysfunction in GD patients. The results showed that miR-363-5p upregulation was significantly associated with the Treg cell dysfunction and inflammatory factors levels in GD patients. Transcriptome sequencing revealed that 883 genes were significantly regulated by miR-363-5p in Treg cells. These genes with significant differential expression were primarily involved in lymphocyte differentiation, immunity, as well as Notch1 and various interleukin signalling pathways. Moreover, miR-363-5p can regulate HSPB1 and Notch1 through the target gene STAT4, thereby regulating Notch1 signalling pathway and inhibiting Treg cells. The effects of miR-363-5p on Treg cell function and STAT4-HSPB1-Notch1 axis were also verified in GD patients. In conclusion, our results indicated that miR-363 could inhibit the proliferation, differentiation and function of Treg cells by regulating the STAT4-HSPB1-Notch1 axis through target gene STAT4. MiR-363-5p may play an important role in Treg cell dysfunction and immune tolerance abnormalities in GD patients.

Indexed as

AdultBiomarkersCell LineCytokinesDisease SusceptibilityFemaleGene Expression ProfilingGene Expression RegulationGraves DiseaseHeat-Shock ProteinsHumansImmunomodulationInflammation MediatorsMaleMicroRNAsMiddle AgedBiomarkersCytokinesHeat-Shock ProteinsHSPB1 protein, humanInflammation MediatorsMicroRNAsMIRN363 microRNA, humanMolecular ChaperonesNOTCH1 protein, humanReceptor, Notch1STAT4 protein, humanSTAT4 Transcription Factorautoimmune diseaseGraves' disease (GD)miR-363-5pregulatory T cells (Tregs)STAT4

Identifiers

PMID34431214
PMCPMC8500983
OpenAlexW3196166735

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.