Evidence map›Paper›PMID 28091531›Full record

ArticleScientific reports2017

TNF-α regulates the proteolytic degradation of ST6Gal-1 and endothelial cell-cell junctions through upregulating expression of BACE1.

Xiao Deng, Jun Zhang, Yan Liu, Linmu Chen, Chao Yu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cerebrovascular Endothelial Dysfunction: Role of BACE1.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. ST6Gal1: Oncogenic signaling pathways and targets.Frontiers in molecular biosciences · 2022
    Review
  10. Review
  11. Article
  12. Is It the Twilight of BACE1 Inhibitors?Current neuropharmacology · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Xiao DengInstitute of Life Science, Chongqing Medical University, Chongqing 400016, P. R. China.
Jun ZhangInstitute of Life Science, Chongqing Medical University, Chongqing 400016, P. R. China.
Yan LiuInstitute of Life Science, Chongqing Medical University, Chongqing 400016, P. R. China.
Linmu ChenInstitute of Life Science, Chongqing Medical University, Chongqing 400016, P. R. China.
Chao YuInstitute of Life Science, Chongqing Medical University, Chongqing 400016, P. R. China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction and monocyte adhesion to vascular endothelial cells are two critical steps in atherosclerosis development, and emerging evidence suggests that protein sialylation is involved in these processes. However, the mechanism underlying this phenomenon remains incompletely elucidated. In this study, we demonstrated that treatment with the proinflammatory cytokine TNF-α disrupted vascular endothelial cell-cell tight junctions and promoted monocyte endothelial cell adhesion. Western blotting and Sambucus nigra lectin (SNA) blotting analyses revealed that TNF-α treatment decreased α-2, 6-sialic acid transferase 1 (ST6Gal-I) levels and downregulated VE-Cadherin α-2, 6 sialylation. Further analysis demonstrated that TNF-α treatment upregulated β-site amyloid precursor protein enzyme 1 (BACE1) expression, thus resulting in sequential ST6Gal-I proteolytic degradation. Furthermore, our results revealed that PKC signaling cascades were involved in TNF-α-induced BACE1 upregulation. Together, these results indicated that the proinflammatory cytokine TNF-α impairs endothelial tight junctions and promotes monocyte-endothelial cell adhesion by upregulating BACE1 expression through activating PKC signaling and sequentially cleaving ST6Gal-I. Thus, inhibition of BACE1 expression may be a new approach for treating atherosclerosis.

Indexed as

ProteolysisAmyloid Precursor Protein SecretasesAntigens, CDAspartic Acid Endopeptidasesbeta-D-Galactoside alpha 2-6-SialyltransferaseCell AdhesionCell LineCell SurvivalEndothelial CellsHumansSialyltransferasesSignal TransductionTight JunctionsTumor Necrosis Factor-alphaUp-RegulationAmyloid Precursor Protein SecretasesAntigens, CDAspartic Acid EndopeptidasesBACE1 protein, humanbeta-D-Galactoside alpha 2-6-SialyltransferaseSialyltransferasesST6GAL1 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID28091531
PMCPMC5238365
OpenAlexW2574585825

What OpenQuestion holds

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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.