Evidence map›Paper›PMID 24572151›Full record

ArticleCardiovascular diabetology2014

High glucose induces human endothelial dysfunction through an Axl-dependent mechanism.

Chien-Hsing Lee, Yi-Shing Shieh, Fone-Ching Hsiao, Feng-Chih Kuo, Chih-Yuan Lin, Chang-Hsun Hsieh, Yi-Jen Hung

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Cardiovascular diabetology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  5. Article
  6. The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
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  15. Article
  16. TAM receptors in cardiovascular disease.Cardiovascular research · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Role of Receptor Tyrosine Kinase Signaling in Renal Fibrosis.International journal of molecular sciences · 2016
    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 at 2 institutions in 1 country.

Chien-Hsing Lee
Yi-Shing Shieh
Fone-Ching Hsiao
Feng-Chih Kuo
Chih-Yuan Lin
Chang-Hsun Hsieh
Yi-Jen HungDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, #325, Section 2, Cheng-Gong Rd,, Nei-Hu, Taipei, Taiwan. metahung@yahoo.com.
Tri-Service General Hospital · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe receptor tyrosine kinase Axl and its ligand growth arrest-specific protein 6 (Gas6) are involved in the diabetic vascular disease. The aim of this study was to explore the role of Gas6/Axl system in high glucose (HG)-induced endothelial dysfunction.

methodsWe investigated the effect of various glucose concentrations on Axl signaling in human microvascular endothelial cells (HMEC-1 s).

resultsHuman plasma Gas6 value inversely correlated with glucose status, endothelial markers. HG decreased Gas6/Axl expression and increased intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in HMEC-1 s. HG significantly decreased HMEC-1 s cell viability and tube formation and promoted monocyte-EC adhesion. Down-regulation of Akt phosphorylation was found in HG culture. Axl transfection significantly reversed HG-induced Akt phosphorylation, VCAM-1 expression and endothelial dysfunction. We also found additive changes in Axl-shRNA-infected HMEC-1 cells in HG culture. Furthermore, Axl overexpression in HMEC-1 s significantly reversed HG-induced vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2) expression. In addition, significantly lower Axl and VEGFR2 expression in arteries were found in diabetic patients as compared with non-diabetic patients.

conclusionsThis study demonstrates that HG can alter Gas6/Axl signaling and may through Akt and VEGF/VEGFR2 downstream molecules and suggests that Gas6/Axl may involve in HG-induced EC dysfunction.

Indexed as

Axl Receptor Tyrosine KinaseCell Line, TransformedCells, CulturedCell SurvivalEndothelium, VascularFemaleGlucoseGrowth Arrest-Specific Protein 6HEK293 CellsHumansIntercellular Signaling Peptides and ProteinsMaleMiddle AgedProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesAXL protein, humanAxl Receptor Tyrosine KinaseGlucoseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinases

Identifiers

PMID24572151
PMCPMC3941696
OpenAlexW2070593926

What OpenQuestion holds

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LicenceCC BY
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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.