Evidence map›Paper›PMID 29568915›Full record

ArticleInternational journal of molecular medicine2018

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model.

Lingcong Wang, Rongbiao Ying, Huifang Jiang, Qun Jin, Jing Kuang, Zhirong Zhang, Ying Shi, Danli Cai, Ruhui Yang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 99% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 4 institutions in 1 country.

Lingcong WangDepartment of ICU, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Rongbiao YingDepartment of Surgical Oncology, Tumor Hospital of Taizhou, Wenling, Zhejiang 317502, P.R. China.
Huifang JiangDepartment of Hematology, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang 310012, P.R. China.
Qun JinDepartment of Pneumology, Zhejiang University International Hospital, Shulan (Hangzhou) Hospital, Hangzhou, Zhejiang 310000, P.R. China.
Jing KuangZhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.
Zhirong ZhangDepartment of ICU, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Ying ShiDepartment of ICU, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Danli CaiDepartment of ICU, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China.
Ruhui YangLishui University, Lishui, Zhejiang 323000, P.R. China.
Zhejiang Chinese Medical University · CNLishui University · CNTongde Hospital of Zhejiang Province · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of the present study was to examine whether aspirin interferes with the inflammatory response in a thrombus‑stimulated lung microvascular endothelial cell (LMVEC) model. The LMVECs were randomly divided into eight groups: Normal group (group N), model group (group M), model + ASP group (group M+A), model+CX3CL1‑short hairpin (sh)RNA group (group M+SH), model + CX3CL1‑overexpression vector group (group M+CX3), model + ASP + shRNA group (group M+A+SH), model + ASP + CX3CL1‑overexpression vector group (group M+A+CX3), and normal + virus control group (group N+V). The endothelial cells were cultured, and a thrombus was added to the cells. Briefly, 12 h following the precipitation of the thrombus, data from ELISA, reverse transcription‑quantitative polymerase chain reaction analysis and confocal microscopy revealed that the levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6, CX3C chemokine ligand 1 (CX3CL1), CX3C chemokine receptor 1 (CX3CR1) and nuclear factor‑κB (NF‑κB) in group M were increased, compared with those in group N (P<0.01). These levels, with the exception of TNF‑α, were significantly lower in group M+SH, compared with those in group M (P<0.01). Furthermore, the levels of IL‑6 in groups M+A, M+CX3 and M+A+CX3 were decreased, compared with those in group M (P<0.01); the level of TNF‑α in group M+A+SH was decreased, compared with that in group M (P<0.01); the level of CX3CR1 waslower in groups M+A and M+A+SH, compared with that in group M (P<0.01), and the level of NF‑κB in group M+SH was decreased, compared with the level in group M and group M+A (P<0.05). In conclusion, the thrombus‑stimulated LMVEC model exhibited induced production of TNF‑α, IL‑6, CX3CL, CX3CR1, NF‑κB and intercellular adhesion molecule‑1. Furthermore, it was confirmed that the signaling pathways involving CX3CL1‑NF‑κB, IL‑6 and TNF‑α were partly inhibited by aspirin.

Indexed as

AnimalsAspirinCells, CulturedChemokine CX3CL1CX3C Chemokine Receptor 1Endothelial CellsEnzyme-Linked Immunosorbent AssayIntercellular Adhesion Molecule-1Interleukin-6LungMaleMicroscopy, ConfocalRatsSignal TransductionThrombosisTumor Necrosis Factor-alphaAspirinChemokine CX3CL1CX3C Chemokine Receptor 1Intercellular Adhesion Molecule-1Interleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID29568915
PMCPMC5881641
OpenAlexW2790139715

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.