Evidence map›Paper›PMID 34350241›Full record

ArticleAnnals of translational medicine2021

Tregs-derived interleukin 35 attenuates endothelial proliferation through STAT1 in pulmonary hypertension.

Naifu Wan, Wuwei Rong, Wentong Zhu, Daile Jia, Peiyuan Bai, Guizhu Liu, Qiangyou Wan, Ankang Lyu

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 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 4 institutions in 1 country.

Naifu WanDepartment of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Wuwei RongDepartment of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Wentong ZhuDepartment of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Daile JiaDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Peiyuan BaiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
Guizhu LiuShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Qiangyou WanShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Ankang LyuDepartment of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ruijin Hospital · CNZhongshan Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo explore the source, the role and the specific mechanism of IL-35 and its downstream molecules in the development of pulmonary hypertension.

methods8-10 weeks male mice were undergoing hypoxia combined with SU5416 (HySu) to establish a pulmonary hypertension (PH) model. The phenotype of PH mice was measured by immunohistochemistry and immunofluorescence staining. The levels of two subunits (EBI3 and p35 subunits) in lung tissue were measured by real-time PCR and western blotting. EBI3 monoclonal antibody was administrated as IL-35 neutralization to offset systemic IL-35 expression. Fludarabine, an inhibitor of STAT1 (signal transducer and activator of transcription 1) was used to clarify the role of STAT1 under IL-35 treatment.

resultsAfter pulmonary hypertension, the expression of IL-35 and its two subunits (EBI3 and p35 subunits) in lung tissue were significantly increased. And the two subunits of IL-35 are highly expressed in Treg cells. Compared with the controlled PH mice, the IL-35 neutralization PH mice showed aggravated pulmonary hypertension phenotype. The specific manifestations are the increase of right ventricular systolic pressure (RVSP), the growing proportion of right heart [RV/(LV+S)], and the remodeling of pulmonary blood vessels increases. The expression of pulmonary vascular endothelium (CD31) in PH mice increased, and the proliferation ability of vascular endothelium enhanced after IL-35 was inhibited. IL-35 phosphorylates STAT1 through the receptor GP130 on pulmonary vascular endothelial cells, which in turn inhibits endothelial cell proliferation. IL-35 recombinant protein can reduce the expression of CD31 in lung tissues of PH mice. But the administration of STAT1 inhibitor made it invalid from the IL-35 effect of reversing pulmonary hypertension.

conclusionsTregs-derived IL-35 can reverse the remodeling of pulmonary blood vessels and alleviate the progression of pulmonary hypertension by reducing the proliferation of endothelial cells.

Indexed as

cardiovascular diseasePulmonary hypertension (PH)

Identifiers

PMID34350241
PMCPMC8263866
OpenAlexW3172942139

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.