Evidence map›Paper›PMID 34863290›Full record

ArticleStem cell research & therapy2021

Genome-wide differential expression profiling of lncRNAs and mRNAs in human induced pluripotent stem cell-derived endothelial cells exposed to e-cigarette extract.

Hoai Huong Thi Le, Chen-Wei Liu, Philip Denaro, Jordan Jousma, Ning-Yi Shao, Irfan Rahman, Won Hee Lee

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Human Primary Mesenchymal Stem Cells Fail to Recover Full Osteogenic Differentiation Potential Following Washout of Electronic Cigarette Aerosol Extracts.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Alteration of the NEpigenomics · 2022
    Article
  11. Review
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

7 authors.

Hoai Huong Thi LeDepartment of Basic Medical Sciences, University of Arizona College of Medicine, 425 N 5th Street, Building ABC1, Rm 426, Phoenix, AZ, 85004-2157, USA.
Chen-Wei LiuDepartment of Basic Medical Sciences, University of Arizona College of Medicine, 425 N 5th Street, Building ABC1, Rm 426, Phoenix, AZ, 85004-2157, USA.
Philip DenaroDepartment of Basic Medical Sciences, University of Arizona College of Medicine, 425 N 5th Street, Building ABC1, Rm 426, Phoenix, AZ, 85004-2157, USA.
Jordan JousmaDepartment of Pharmacology and Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL, 60612, USA.
Ning-Yi ShaoHealth Sciences, University of Macau, Macau, China.
Irfan RahmanDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Won Hee LeeDepartment of Basic Medical Sciences, University of Arizona College of Medicine, 425 N 5th Street, Building ABC1, Rm 426, Phoenix, AZ, 85004-2157, USA. whlee@arizona.edu.ORCID 0000-0001-8534-9639

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElectronic-cigarette (e-cig) usage, particularly in the youth population, is a growing concern. It is known that e-cig causes endothelial dysfunction, which is a risk factor for the development of cardiovascular diseases; however, the mechanisms involved remain unclear. We hypothesized that long noncoding RNAs (lncRNAs) may play a role in e-cig-induced endothelial dysfunction.

methodsHere, we identified lncRNAs that are dysregulated in human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) following 24 h of e-cig aerosol extract treatment via microarray analysis. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analyses of the dysregulated mRNAs following e-cig exposure and constructed co-expression networks of the top 5 upregulated lncRNAs and the top 5 downregulated lncRNAs and the mRNAs that are correlated with them. Furthermore, the functional effects of knocking down lncRNA lung cancer-associated transcript 1 (LUCAT1) on EC phenotypes were determined as it was one of the significantly upregulated lncRNAs following e-cig exposure based on our profiling.

results183 lncRNAs and 132 mRNAs were found to be upregulated, whereas 297 lncRNAs and 413 mRNAs were found to be downregulated after e-cig exposure. We also observed that e-cig caused dysregulation of endothelial metabolism resulting in increased FAO activity, higher mitochondrial membrane potential, and decreased glucose uptake and glycolysis. These results suggest that e-cig alters EC metabolism by increasing FAO to compensate for energy deficiency in ECs. Finally, the knockdown of LUCAT1 prevented e-cig-induced EC dysfunction by maintaining  vascular barrier, reducing reactive oxygen species level, and increasing migration capacity.

conclusionThis study identifies an expression profile of differentially expressed lncRNAs and several potential regulators and pathways in ECs exposed to e-cig, which provide insights into the regulation of lncRNAs and mRNAs and the role of lncRNA and mRNA networks in ECs associated e-cig exposure.

Indexed as

E-Cigarette VaporElectronic Nicotine Delivery SystemsInduced Pluripotent Stem CellsRNA, Long NoncodingRNA, MessengerEndothelial CellsGene Expression ProfilingGene OntologyGene Regulatory NetworksHumansE-Cigarette VaporRNA, Long NoncodingRNA, Messengere-cigarettesendothelial dysfunctionfatty acid oxidationiPSC-ECslncRNAs

Identifiers

PMID34863290
PMCPMC8643021

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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.