Evidence map›Paper›PMID 26714823›Full record

ArticleJournal of physiology and biochemistry2016

Serum amyloid A stimulates vascular endothelial growth factor receptor 2 expression and angiogenesis.

Mei Lv, Yan-fei Xia, Bo Li, Hui Liu, Jin-yu Pan, Bei-bei Li, Cheng Zhang, Feng-shuang An

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  14. Article
  15. Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019
    Review
  16. Review
  17. 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

8 authors at 2 institutions in 1 country.

Mei LvQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Yan-fei XiaDepartment of Ultrasound, Shandong Provincial Hospital, Ji'nan, People's Republic of China.
Bo LiQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Hui LiuQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Jin-yu PanQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Bei-bei LiQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Cheng ZhangQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China.
Feng-shuang AnQilu Hospital of Shandong University, Ji'nan, Shandong, 250012, People's Republic of China. AnFengShuang@yeah.net.
Qilu Hospital of Shandong University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum amyloid A (SAA), a major acute-phase reactant, modulates angiogenesis in many diseases. Vascular endothelial growth factor receptor 2 (VEGFR2) is the primary angiogenic receptor for vascular endothelial growth factor (VEGF), but the possibility of an interaction between SAA and VEGFR2 has not yet been resolved. Here, we investigated if SAA stimulates the expression of VEGFR2 and promotes angiogenesis in vitro. Human umbilical vein endothelial cells (HUVECs) were stimulated with recombinant SAA (rSAA), and the messenger RNA (mRNA) and protein expression of VEGFR2 was detected by Western blot analysis and quantitative real-time PCR. Formyl peptide receptor-like 1 (FPRL1) agonist (WKYMVm) and antagonist (WRW(4)) and inhibitors of mitogen-activated protein kinases (MAPKs) were used to investigate the mechanism of regulation of VEGFR2.We show that SAA induces VEGFR2 expression in a time- and dose-dependent manner in HUVECs. In addition, SAA promotes tube formation in HUVECs. The effect of SAA on tube formation was shown to be the result of an increase in VEGFR2 expression, which was blocked by the multi-angiokinase receptor inhibitor BIBF1120. These activities of SAA appear to be mediated by FPRL1/MAPK signaling pathways, as they were mimicked by WKYMVm and abrogated by WRW(4) and inhibitors of MAPKs. These observations indicate that SAA induces VEGFR2 expression and promotes tube formation in HUVECs via the FPRL1/MAPK signaling pathway, thus providing a potential target for the control of angiogenesis.

Indexed as

Neovascularization, PhysiologicHumansHuman Umbilical Vein Endothelial CellsSerum Amyloid A ProteinVascular Endothelial Growth Factor Receptor-2Serum Amyloid A ProteinVascular Endothelial Growth Factor Receptor-2AngiogenesisFPRL1MAPKSAAVEGFR2

Identifiers

PMID26714823
OpenAlexW2207213492

What OpenQuestion holds

Textmetadata
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.