Evidence map›Paper›PMID 36705405›Full record

ArticleImmunity, inflammation and disease2023

lncRNA NEAT1/miR-495-3p regulates angiogenesis in burn sepsis through the TGF-β1 and SMAD signaling pathways.

Yanbin Meng, Zhenming Hao, Hairui Zhang, Peiyi Bai, Wanli Guo, Xiaorui Tian, Jun Xu

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Yanbin MengFirst Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
Zhenming HaoBurn Department, Burn and Plastic Center of General Hospital of TISCO (Shanxi Burn Treatment Center), Taiyuan, Shanxi, China.
Hairui ZhangBurn Department, Burn and Plastic Center of General Hospital of TISCO (Shanxi Burn Treatment Center), Taiyuan, Shanxi, China.
Peiyi BaiBurn Department, Burn and Plastic Center of General Hospital of TISCO (Shanxi Burn Treatment Center), Taiyuan, Shanxi, China.
Wanli GuoBurn Department, Burn and Plastic Center of General Hospital of TISCO (Shanxi Burn Treatment Center), Taiyuan, Shanxi, China.
Xiaorui TianWound Repair Department, Burn and Plastic Center of General Hospital of TISCO (Shanxi Burn Treatment Center), Taiyuan, Shanxi, China.
Jun XuDepartment of General Surgery, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.ORCID 0000-0002-6868-5945
Burn Institute · USShanxi Medical University · CNTaiyuan Iron and Steel Group (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTo investigate the role of the long-chain noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) in the process of angiogenesis in human umbilical vein endothelial cells (HUVECs) and illustrate its potential role in burn sepsis (BS) pathogenesis.

methodsHUVECs were treated with BS patient serum or healthy control serum. NEAT1 shRNA, miR-495-3p mimics, and miR-495-3p inhibitor were transfected into HUVECs. NEAT1 and miR-495-3 levels in serum or HUVECs were detected using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 and flow cytometry assays were used to explore the proliferation and apoptosis of HUVECs. The expression of vascular endothelial growth factor (VEGF) in the supernatant was detected using enzyme-linked immunosorbent assay. Tube formation of HUVECs was also analyzed. Western blot analysis was used to analyze signaling pathway proteins.

resultsIn HUVECs stimulated with BS patient serum, NEAT1 expression was increased, while miR-495-3p expression was decreased. In addition, NEAT1 silencing by specific shRNA inhibited cell proliferation, VEGF production, and tube formation under burn patient serum treatment, which decreased the TGFβ1/SMAD signaling pathway activation. Moreover, miR-495-3p minics inhibited angiogenesis and the activation of signaling pathways induced by NEAT1 shRNA. Furthermore, miR-495-3p inhobitor promoted angiogenesis in HUVECs and activated the TGFβ1/SMAD signaling pathway. In patients with BS, NEAT1 expression was significantly increased and miR-495-3p expression was decreased compared to healthy controls, and NEAT1 and miR-495-3p expression was associated with the clinical features of patients.

conclusionsOur results indicate that lncRNA NEAT1 regulates angiogenesis and activates the TGFβ1/SMAD signaling pathway during the occurrence of BS.

Indexed as

BurnsMicroRNAsRNA, Long NoncodingSepsisHumansHuman Umbilical Vein Endothelial CellsRNA, Small InterferingSignal TransductionTransforming Growth Factor beta1Vascular Endothelial Growth Factor AMicroRNAsMIRN495 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingRNA, Small InterferingTransforming Growth Factor beta1Vascular Endothelial Growth Factor Aangiogenesisburn sepsismiR-495-3pNEAT1

Identifiers

PMID36705405
PMCPMC9841715
OpenAlexW4316469384

What Socratic 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 Socratic graph.