Evidence map›Paper›PMID 35066809›Full record

ArticleGenes & genomics2022

LncRNA-GAS5/miR-382-3p axis inhibits pulmonary artery remodeling and promotes autophagy in chronic thromboembolic pulmonary hypertension.

Xiaona Feng, Kaifeng Wang, Ting Yang, Yanhui Liu, Xiaodong Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Genes & genomics, 2022. 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
1.3field-weighted citation impact, top 21% 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, 15 citations in OpenAlex.

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  10. Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024
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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

5 authors at 1 institution in 1 country.

Xiaona FengDepartment of Obstetrics and Gynecology, First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang, China.
Kaifeng WangVascular Surgery, First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang, China. wkf_wangkf@163.com.
Ting YangVascular Surgery, First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang, China.
Yanhui LiuVascular Surgery, First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang, China.
Xiaodong WangVascular Surgery, First Affiliated Hospital of Jiamusi University, No. 348, Dexiang Street, Xiangyang District, Jiamusi, 154002, Heilongjiang, China.
First Affiliated Hospital of Jiamusi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe have clarified the role of miR-382-3p in chronic thromboembolic pulmonary hypertension (CTEPH), but what is less clear lies in its upstream regulatory mechanism.

objectiveTo explore the regulation mechanism of GAS5/miR-382-3p axis on CTEPH.

methodsIn vitro, we constructed cell models by treating Pulmonary Artery Smooth Muscle Cells (PASMCs) with platelet-derived growth factor-BB (PDGF-BB). The effects of different concentrations of PDGF-BB on the activity of PASMCs were tested by cell counting kit-8 (CCK-8). The upstream lncRNA of miR-382-3p was screened and confirmed through bioinformatics analysis, RNA pull-down, quantitative reverse transcription polymerase chain reaction (qRT-PCR), dual luciferase reporter gene and RNA immunoprecipitation assays. The effects of GAS5/miR-382-3p axis on the viability, migration, and expressions of autophagy- and angiogenesis-related proteins were confirmed by rescue experiments (CCK-8, wound healing and western blot). In vivo, animal models by perfusing autologous blood vessels, the effects of GAS5 overexpression or silencing on the expressions of miR-382-3p, angiogenesis- and autophagy-related genes, mean pulmonary arterial pressure (mPAP) and pulmonary artery wall were determined by biological signal acquisition system, hematoxylin-eosin staining, qRT-PCR and western blot.

resultsPDGF-BB dose-dependently promoted PASMCs viability. XIST and GAS5 expressions in PASMCs were affected by the concentration of PDGF-BB, but only GAS5 can be pulled down by miR-382-3p probe. GAS5 targeted miR-382-3p to inhibit the viability and migration of PAMSCs, mPAP in CTEPH rats, pulmonary artery wall thickening and angiogenesis, and promote autophagy.

conclusionsGAS5/miR-382-3p axis is involved in the regulation of pulmonary artery remodeling and autophagy in CTEPH.

Indexed as

Hypertension, PulmonaryMicroRNAsPulmonary ArteryRNA, Long NoncodingAnimalsAutophagyBecaplerminHumansRatsBecaplerminGAS5 long non-coding RNA, humanMicroRNAsMIRN382 microRNA, humanRNA, Long NoncodingAutophagyChronic thromboembolic pulmonary hypertensionLong non-coding RNA GAS5miR-382-3p

Identifiers

PMID35066809
OpenAlexW4206960050

What OpenQuestion holds

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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.