Evidence map›Paper›PMID 25793984›Full record

ArticlePloS one2015

Low shear stress induced HMGB1 translocation and release via PECAM-1/PARP-1 pathway to induce inflammation response.

Wei-dong Qin, Shao-hua Mi, Chen Li, Gui-xia Wang, Jian-ning Zhang, Hao Wang, Fan Zhang, Yang Ma, Da-wei Wu, Mingxiang Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-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

19 citing papers in PubMed, 42 citations in OpenAlex.

  1. The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
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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

10 authors at 2 institutions in 1 country.

Wei-dong QinThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Shao-hua MiThe Department of Cardiology, Yu Huang Ding Hospital, Yantai, Shandong, China.
Chen LiThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Gui-xia WangThe Department of Radiology, Linyi People's Hospital, Linyi, Shandong, China.
Jian-ning ZhangThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Hao WangThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Fan ZhangThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Yang MaThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Da-wei WuThe Department of Critical Care Unit, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Mingxiang ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Qilu Hospital of Shandong University · CNLinyi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low shear stress (LSS) plays a critical role in the site predilection of atherosclerosis through activation of cellular mechanosensors, such as platelet endothelial cell adhesion molecule 1 (PECAM-1). Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that regulates the expression of various inflammatory cytokines. The nuclear enzyme high mobility group box 1 (HMGB1) can induce inflammation response by binding to toll-like receptor 4 (TLR4). In the present study, we aimed to investigate the role and mechanism of HMGB1 in LSS induced inflammation in human umbilical vein endothelial cells (HUVECs). HUVECs were stimulated by undisturbed shear stress (USS, 1 Pa) and LSS (0.4 Pa) in our experiments. Gene expression was inhibited by small interfering RNA (siRNA). ICAM-1 expression was regulated by LSS in a time dependent manner. LSS can induce HMGB1 translocation from nucleus to cytoplasm and release. Compared with the USS, LSS could increase the protein expression of PECAM-1 and PARP-1 as well as the secretion of TNF-α and IL-1β. LSS induced the translocation of HMGB1 from nucleus to cytoplasm. Inhibition of HGMB1 reduced LSS-induced inflammatory response. Inhibition of PARP-1 suppressed inflammatory response through inhibiting TLR4 expression and HMGB1 translocation. PECAM-1 inhibition reduced LSS-induced ICAM-1 expression, TNF-α and IL-1β secretion, and monocytes adhesion. LSS can induce inflammatory response via PECAM-1/PARP-1/HMGB1 pathway. PARP-1 plays a fundamental role in HMGB1 translocation and TLR4 expression. Inhibition of PARP-1 may shed light on the treatment of HMGB1 involved inflammation during atherosclerosis.

Indexed as

Shear StrengthSignal TransductionStress, MechanicalHMGB1 ProteinHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1Interleukin-1betaPlatelet Endothelial Cell Adhesion Molecule-1Poly(ADP-ribose) PolymerasesProtein TransportTime FactorsToll-Like Receptor 4Tumor Necrosis Factor-alphaUp-RegulationHMGB1 ProteinIntercellular Adhesion Molecule-1Interleukin-1betaPlatelet Endothelial Cell Adhesion Molecule-1Poly(ADP-ribose) PolymerasesToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID25793984
PMCPMC4368774
OpenAlexW2085035343

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.