Evidence map›Paper›PMID 34130625›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

LncRNA H19 induces immune dysregulation of BMMSCs, at least partly, by inhibiting IL-2 production.

Xinpeng Chen, Xiuxia Luo, Yazhi Wei, Hualin Sun, Liping Dai, Yidou Tangzhou, Huijie Jin, Zhihua Yin

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.0field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Xinpeng ChenRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Xiuxia LuoRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Yazhi WeiRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Hualin SunRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Liping DaiRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Yidou TangzhouRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Huijie JinRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China.
Zhihua YinRheumatology Department, Shenzhen Futian Hospital for Rheumatic Diseases, Nonglin Road 22#, Futian District, Shenzhen, 518040, Guangdong, China. zhihuayinshenzhen@163.com.ORCID 0000-0003-3537-8268
Fourth People's Hospital of Shenzhen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is a representative systemic autoimmune disease. LncRNA H19 has been identified to participate in various biological processes in human diseases. However, the role of H19 in SLE remains unclear.

methodsIn this study, we first examined H19 expression in SLE patients by RT-qPCR and found that H19 expression was significantly upregulated in the serum and bone marrow-derived mesenchymal stem cells (BMMSCs) of SLE patients and positively associated with SLE disease activity index. We then performed gain-of-function and loss-of-function using mimic-H19 (H19-OE) and inhibitor-H19 (H19-KD) to examine the effects of H19 on BMMSC differentiation, proliferation, migration, and apoptosis using flow cytometry, DAPI staining, and migration and apoptosis assays.

resultsThe results showed that H19 inhibited proliferation and migration but promoted apoptosis of BMMSCs, interfered with BMMSCs-mediated Treg cell proliferation and differentiation, and regulated BMMSCs-mediated Tfh/Treg cell balance. Dual-luciferase reporter assay confirmed the in silico prediction of interaction between H19 and IL-2. Furthermore, RT-qPCR showed that H19 directly inhibited IL-2 transcription in BMMSCs. ELISA showed that both active and total IL-2 protein levels were significantly lower in SLE BMMSCs. More importantly, we found that IL-2 significantly enhanced H19-OE-induced Treg cell differentiation and migration of BMMSCs, and these effects were reversed by anti-IL-2 antibody.

conclusionOverall, our study indicates that LncRNA H19 induces immune dysregulation of BMMSCs, at least partly, by inhibiting IL-2 production and might be a novel therapeutic target for SLE.

Indexed as

Gene Expression RegulationApoptosisBiomarkersCase-Control StudiesCell DifferentiationCell MovementCells, CulturedCoculture TechniquesDisease SusceptibilityHumansImmunomodulationInterleukin-2Leukocytes, MononuclearLupus Erythematosus, SystemicMesenchymal Stem CellsRNA, Long NoncodingBiomarkersH19 long non-coding RNAInterleukin-2RNA, Long NoncodingIL-2Immune regulationlncRNA H19Systemic lupus erythematosus

Identifiers

PMID34130625
PMCPMC8207721
OpenAlexW3170856515

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.