Evidence map›Paper›PMID 35596131›Full record

ArticleCellular & molecular biology letters2022

HCMV-miR-US33-5p promotes apoptosis of aortic vascular smooth muscle cells by targeting EPAS1/SLC3A2 pathway.

Jian Dong, Shuangshuang Li, Zilin Lu, Pengcheng Du, Guangqin Liu, Mintao Li, Chao Ma, Jian Zhou, Junmin Bao

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 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
4.7field-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, 30 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Infection and immunity · 2024
    Article
  7. Article
  8. Article
  9. IPCellular & molecular biology letters · 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

9 authors at 4 institutions in 1 country.

Jian Dong *Department of Vascular Surgery, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. dr_dongj@163.com.
Shuangshuang Li *Department of Vascular Surgery, Changhai Hospital, Navy Medical University, Shanghai, China.
Zilin Lu *School of Health Science and Engineering, University of Shanghai for Science Technology, Shanghai, China.
Pengcheng DuDepartment of Vascular Surgery, Changhai Hospital, Navy Medical University, Shanghai, China.
Guangqin LiuDepartment of Vascular Surgery, Changhai Hospital, Navy Medical University, Shanghai, China.
Mintao LiDepartment of Vascular Surgery, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Chao MaDepartment of Vascular Surgery, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Jian ZhouDepartment of Vascular Surgery, Changhai Hospital, Navy Medical University, Shanghai, China. zhoujian1-2@163.com.
Junmin BaoDepartment of Vascular Surgery, Changhai Hospital, Navy Medical University, Shanghai, China. baojm@189.cn.
Changhai Hospital · CNShanghai University of Traditional Chinese Medicine · CNSecond Military Medical University · CNUniversity of Shanghai for Science and Technology · CN

Funding

National Natural Science Foundation Youth Fund 81700434Science and Technology Commission of Shanghai Municipality 19ZR1478300
6 · The paper itself

Abstract

backgroundIn patients with acute aortic dissection (AAD), increased vascular smooth muscle cell (VSMC) apoptosis has been found. Human cytomegalovirus (HCMV)-miR-US33-5p was significantly increased in the plasma of patients with AAD. However, the roles of miR-US33-5p in human aortic VSMC (HA-VSMC) apoptosis remain to be elucidated.

methodsIn the current study, cell apoptosis was analyzed by flow cytometry, cell proliferation by CCK-8 assay, and differentially expressed genes by RNA sequencing. Luciferase reporter assay was used for binding analysis between miR-US33-5p and endothelial PAS domain protein 1 (EPAS1), and EPAS1 and amino acid transporter heavy chain, member 2 (SLC3A2). The enrichment degree of SLC3A2 promoter DNA was analyzed by chromatin immunoprecipitation assay. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and immunoblotting were performed for measuring messenger RNA (mRNA) and protein levels, respectively.

resultsIt was found that HCMV infection inhibited proliferation but promoted HA-VSMC apoptosis by upregulating HCMV-miR-US33-5p. Transfection of HCMV-miR-US33-5p mimics the significant effect on several signaling pathways including integrin signaling as shown in the RNA sequencing data. Western blotting analysis confirmed that HCMV-miR-US33-5p mimics suppression of the activity of key factors of the integrin signal pathway including FAK, AKT, CAS, and Rac. Mechanistic study showed that HCMV-miR-US33-5p bound to the 3'-untranslated region of EPAS1 to suppress its expression, leading to suppression of SLC3A2 expression, which ultimately promoted cell apoptosis and inhibited cell proliferation. This was confirmed by the findings that silencing EPAS1 significantly reduced the SLC3A2 expression and inhibited proliferation and key factors of integrin signal pathway.

conclusionsHCMV-miR-US33-5p suppressed proliferation, key factors of integrin signal pathway, and EPAS1/SLC3A2 expression, but promoted HA-VSMC apoptosis. These findings highlighted the importance of HCMV-miR-US33-5p/EPAS1/SCL3A2 signaling and may provide new insights into therapeutic strategies for AAD.

Indexed as

Aortic DissectionCytomegalovirusMicroRNAsMyocytes, Smooth MuscleApoptosisBasic Helix-Loop-Helix ProteinsCell ProliferationEndothelial PAS Domain-Containing Protein 1Fusion Regulatory Protein 1, Heavy ChainHumansIntegrinsMuscle, Smooth, VascularBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Fusion Regulatory Protein 1, Heavy ChainIntegrinsMicroRNAsSLC3A2 protein, humanAcute aortic dissectionAortic vascular smooth muscle cellsApoptosisEndothelial PAS domain protein 1miRNAsSLC3A2

Identifiers

PMID35596131
PMCPMC9123696
OpenAlexW4280517847

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.