Evidence map›Paper›PMID 24722573›Full record

ArticleInternational journal of molecular sciences2014

Vasostatin inhibits VEGF-induced endothelial cell proliferation, tube formation and induces cell apoptosis under oxygen deprivation.

Qun Shu, Wenjiao Li, Haichuan Li, Gang Sun

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Anti-Tumor Effect of Parasitic Protozoans.Bioengineering (Basel, Switzerland) · 2022
    Review
  4. Application Progress of Organoids in Colorectal Cancer.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Involvement of activation of C-met signaling pathway in CD151-induced HUVECs angiogenesis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
  11. Functional roles of calreticulin in cancer biology.BioMed research international · 2015
    Review
  12. 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

4 authors at 2 institutions in 1 country.

Qun ShuShanghai Changning Maternity and Infant Health Hospital, 773 Wuyi Road, Shanghai 200051, China. cmihh2012@163.com.
Wenjiao LiShanghai Changning Maternity and Infant Health Hospital, 773 Wuyi Road, Shanghai 200051, China. liwenjiao2008@163.com.
Haichuan LiShanghai Changning Maternity and Infant Health Hospital, 773 Wuyi Road, Shanghai 200051, China. lihaichuan_happy@163.com.
Gang SunSchool of Life Sciences, Fudan University, 220 Handan Road, Shanghai 200433, China. sungang122012@163.com.
Shanghai Changning Maternity and Infant Health Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-angiogenesis treatment has been a promising new form of cancer therapy. Endothelial cells are critical for vascular homeostasis and play important roles in angiogenesis, vascular and tissue remodeling. Vasostatin, the 180 amino acid N-terminal fragment of the calreticulin protein, is reported to be a potent endogenous inhibitor of angiogenesis, suppressing tumor growth. However, the mechanism of these effects has not been sufficiently investigated. This study was performed to investigate the possible mechanism of vasostatin effects on primary cultured human umbilical vein endothelial cells (HUVEC). We found that vasostatin could inhibit the cell viability of HUVEC and induce cell apoptosis through mitochondrial pathways via activation of caspase-3 under oxygen deprivation conditions. Meanwhile, vasostatin also inhibited vascular endothelial growth factor-induced proliferation and tube formation of HUVEC. The possible mechanism of vasostatin-inhibited proliferation of HUVEC could be through down-regulation of endothelial nitric oxide synthase. These findings suggest that vasostatin could regulate endothelial cell function and might be used in anti-angiogenesis treatment.

Indexed as

Apoptosisbcl-2-Associated X ProteinCalreticulinCaspase 3Cell ProliferationCells, CulturedDown-RegulationHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PhysiologicNitric Oxide Synthase Type IIIOxygenPeptide FragmentsProto-Oncogene Proteins c-bcl-2Vascular Endothelial Growth Factor Abcl-2-Associated X ProteinCalreticulinCaspase 3Nitric Oxide Synthase Type IIIOxygenPeptide FragmentsProto-Oncogene Proteins c-bcl-2Vascular Endothelial Growth Factor Avasostatin

Identifiers

PMID24722573
PMCPMC4013612
OpenAlexW2113080661

What OpenQuestion holds

Textmetadata
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.