Evidence map›Paper›PMID 24505433›Full record

ArticlePloS one2014

Effect and mechanism of thrombospondin-1 on the angiogenesis potential in human endothelial progenitor cells: an in vitro study.

Qing Qin, Juying Qian, Lei Ge, Li Shen, Jianguo Jia, Jianhao Jin, Junbo Ge

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Identification of CD141Stem cell research & therapy · 2024
    Article
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  8. CD47 signaling pathways controlling cellular differentiation and responses to stress.Critical reviews in biochemistry and molecular biology · 2015
    Review
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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

7 authors at 3 institutions in 1 country.

Qing QinShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Juying QianShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Lei GeShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Li ShenShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Jianguo JiaShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Jianhao JinShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Junbo GeShanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.
Sun Yat-sen University · CNZhongshan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCoronary collateral circulation plays a protective role in patients with coronary artery disease (CAD). We investigated whether thrombospondin-1(TSP-1) has an inhibitory effect on angiogenesis potential in endothelial progenitor cells(EPCs) and tested whether TSP-1 are altered in plasma of patients who had chronic total occlusion (CTO) in at least one coronary artery and with different collateral stages(according to Rentrop grading system). METHODS AND

resultsWe isolated early and late EPCs from human cord blood and investigated a dose-dependent effect of TSP-1 on their angiogenesis potential by Matrigel angiogenesis assay. We found that TSP-1 (5 µg/ml) inhibited early EPCs incorporation into tubules after pretreatment for 1, 6 and 12 hours, respectively (83.3±11.9 versus 50.0±10.1 per field for 1 hour,161.7±12.6 versus 124.0±14.4 for 6 hours, 118.3±12.6 versus 68.0±20.1 for 12 hours, p<0.05). TSP-1 also inhibited late EPCs tubule formation at 1 µg/ml (6653.4±422.0 µm/HPFversus 5552.8±136.0 µm/HPF, p<0.05), and the inhibition was further enhanced at 5 µg/ml (6653.4±422.0 µm/HPF versus 2118.6±915.0 µm/HPF p<0.01). To explore the mechanism involved, a small interfering RNA was used. In vitro, CD47 siRNA significantly attenuated TSP-1's inhibition of angiogenesis on late EPCs and similar results were obtained after functional blocking by anti-CD47 antibody. Then we investigated pathways downstream of CD47 and found TSP-1 regulated VEGF-induced VEGFR2 phosphorylation via CD47. Furthermore, we examined plasma TSP-1 levels in patients with CTO who developed different stages of collaterals and found a paradoxical higher level of TSP-1 in patients with good collaterals compared with bad ones (612.9±554.0 ng/ml versus 224.4±132.4 ng/ml, p<0.05).

conclusionTSP-1 inhibited angiogenesis potential of early and late EPCs in vitro. This inhibition may be regulated by TSP-1's interaction with CD47, resulting in down regulation of VEGFR2 phosphorylation. In patients with CTO, there may be a self-adjustment mechanism in bad collaterals which is shown as low level of angiogenesis inhibitor TSP-1, and thus favoring collateral formation.

Indexed as

Neovascularization, PhysiologicAdultAgedCD47 AntigenCells, CulturedEndothelial CellsFemaleHumansMaleMiddle AgedStem CellsThrombospondin 1Vascular Endothelial Growth Factor Receptor-2CD47 AntigenKDR protein, humanThrombospondin 1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID24505433
PMCPMC3914943
OpenAlexW2066412990

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.