Evidence map›Paper›PMID 39433980›Full record

ArticleJournal of cellular and molecular medicine2024

Dendritic cell-derived lncRNAs in patients with acute coronary syndrome.

Zhenglong Wang, K E Changhao, Yuheng Chen, Yongchao Zhao, Yuanjie He, Xiao Liang, Qingxian Tu, Min Xu, Fujia Guo, Junbo Ge and 1 more

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Dendritic cell-derived lncRNAs in patients with acute coronary syndrome.Journal of cellular and molecular medicine · 2024
    Article
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

11 authors.

Zhenglong WangDepartment of Cardiology, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.ORCID 0000-0002-4860-540X
K E ChanghaoDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Yuheng ChenDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Yongchao ZhaoDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Yuanjie HeDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Xiao LiangDepartment of Cardiology, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Qingxian TuDepartment of Cardiology, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Min XuDepartment of Cardiology, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Fujia GuoDepartment of Cardiology, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Junbo GeDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Bei ShiDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.

Funding

National Natural Science Foundation of China
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) and dendritic cells (DC) play crucial roles in the development of acute coronary syndrome (ACS); however, the mechanisms remain unclear. To investigate this, we analysed the differentially expressed lncRNAs in monocyte-derived DCs (moDCs) from patients with ACS. Peripheral blood mononuclear cells were transformed into moDCs. Cellular morphology and expression levels of moDC-specific markers (CD80, CD86, CD11c, CD14 and HLA-DR) were analysed using electron microscopy (EM) and flow cytometry (FCM), respectively. Differentially expressed lncRNAs and their functions were predicted using gene sequencing, gene ontology and the Kyoto Encyclopedia of Genes and Genomes. The expression levels of markers, signalling pathway molecules (p-PI3K and p-AKT), inflammatory cytokines (IL-6 and IL-12p70) and target gene (C-C motif chemokine ligand (CCL) 15 and CCL14) were analysed by overexpression or silencing of candidate lncRNAs. EM revealed the cells to be suspended in dendritic pseudopodia. CD11c and HLA-DR were upregulated, while CD80 and CD86 were downregulated. Comparison between the UA versus ST group showed the highest number of differentially expressed lncRNAs (n = 113), followed by UA versus NST (n = 115), CON versus NST (n = 49) and CON versus ST (n = 35); however, the number was low for CON versus UA and ST versus NST groups. moDC-specific marker expression, signalling pathway molecules, inflammatory cytokines and CCL14 were upregulated following lentiviral overexpression of smart silencer-CCL15-CCL14; however, expression levels decreased following transfection with siRNA. The morphology, function and lncRNA expression of moDCs differ depending on the type of ACS. The differentially expressed lncRNAs, particularly CCL15-CCL14, regulate the function of moDCs. Thus, our study provides new insights regarding the role of lncRNAs in ACS and indicates the potential use of CCL15-CCL14 as a novel diagnostic marker and therapeutic target.

Indexed as

Acute Coronary SyndromeDendritic CellsRNA, Long NoncodingAgedBiomarkersCytokinesFemaleGene Expression ProfilingGene Expression RegulationHumansMaleMiddle AgedSignal TransductionBiomarkersCytokinesRNA, Long Noncodingacute coronary syndromegene sequencinglong non‐coding RNAmonocyte‐derived dendritic cellspathogenesis

Identifiers

PMID39433980
PMCPMC11493550

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.