Evidence map›Paper›PMID 36307990›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023

Polyamines from myeloid-derived suppressor cells promote Th17 polarization and disease progression.

Cong Hu, Yu Zhen, Zhanchuan Ma, Li Zhao, Hao Wu, Chang Shu, Bo Pang, Jinyu Yu, Ying Xu, Xin Zhang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  14. Coenzyme Q10 Stimulate Reproductive Vatality.Drug design, development and therapy · 2023
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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

12 authors at 4 institutions in 2 countries.

Cong HuCentral Laboratory, The First Hospital of Jilin University, Changchun 130021, China; Key Laboratory of Organ Regeneration and Transplantation, Ministry of Education, Changchun 130021, China; Center for Reproductive Medicine, Center for Prenatal Diagnosis, The First Hospital of Jilin University, Changchun 130021, China.
Yu ZhenDepartment of Dermatology, The First Hospital of Jilin University, Changchun, China.
Zhanchuan MaCentral Laboratory, The First Hospital of Jilin University, Changchun 130021, China; Key Laboratory of Organ Regeneration and Transplantation, Ministry of Education, Changchun 130021, China.
Li ZhaoBethune Institute of Epigenetic Medicine, The First Hospital, Jilin University, Changchun 130021, China.
Hao WuDepartment of Nephrology, The First Hospital of Jilin University, Changchun 130021, China.
Chang ShuDepartment of Obstetrics and Gynecology, The First Hospital of Jilin University, Changchun 130021, China.
Bo PangCentral Laboratory, The First Hospital of Jilin University, Changchun 130021, China; Department of Cardiology, The First Hospital of Jilin University, Changchun, China.
Jinyu YuDepartment of Urology, The First Hospital of Jilin University, Changchun 130021, China.
Ying XuDepartment of Nephrology, The First Hospital of Jilin University, Changchun 130021, China.
Xin ZhangDepartment of Rheumatology and Immunology, China-Japan Union Hospital of Jilin University, Changchun 130021, China.
Xiang-Yang WangDepartment of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
Huanfa YiCentral Laboratory, The First Hospital of Jilin University, Changchun 130021, China; Key Laboratory of Organ Regeneration and Transplantation, Ministry of Education, Changchun 130021, China. Electronic address: yihuanfa@jlu.edu.cn.
Jilin University · CNMinistry of Education of the People's Republic of China · CNFirst Bethune Hospital of Jilin University · CNVirginia Commonwealth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are a group of immature myeloid cells that play an important role in diseases. MDSCs promote Th17 differentiation and aggravate systemic lupus erythematosus (SLE) progression by producing arginase-1 to metabolize arginine. However, the metabolic regulators remain unknown. Here, we report that MDSC derivative polyamines can promote Th17 differentiation via miR-542-5p in vitro. Th17 polarization was enhanced in response to polyamine treatment or upon miR-542-5p overexpression. The TGF-β/SMAD3 pathway was shown to be involved in miR-542-5p-facilitated Th17 differentiation. Furthermore, miR-542-5p expression positively correlated with the levels of polyamine synthetases in peripheral blood mononuclear cells of patients with SLE as well as disease severity. In humanized SLE model mice, MDSC depletion decreased the levels of Th17 cells, accompanied by reduced expression of miR-542-5p and these polyamine synthetases. In addition, miR-542-5p expression positively correlated with the Th17 level and disease severity in both patients and humanized SLE mice. Together, our data reveal a novel molecular pathway by which MDSC-derived polyamine metabolism enhances Th17 differentiation and aggravates SLE.

Indexed as

Lupus Erythematosus, SystemicMicroRNAsMyeloid-Derived Suppressor CellsAnimalsDisease ProgressionLeukocytes, MononuclearLigasesMiceTh17 CellsLigasesMicroRNAsmiR-542-5pmyeloid-derived suppressor cellspolyaminesystemic lupus erythematosusTGF-β/SMAD3Th17

Identifiers

PMID36307990
PMCPMC9931554
OpenAlexW4307457912

What OpenQuestion 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 OpenQuestion graph.