Evidence map›Paper›PMID 20500895›Full record

ArticleBMC cell biology2010

Angiotensin II upregulates the expression of placental growth factor in human vascular endothelial cells and smooth muscle cells.

Pingxi Pan, Hua Fu, Lingjun Zhang, He Huang, Fengming Luo, Wenchao Wu, Yingqiang Guo, Xiaojing Liu

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
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  8. Review
  9. Placental growth factor blunts uterine artery responses to angiotensin II.BJOG : an international journal of obstetrics and gynaecology · 2019
    Article
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  15. Observational
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  19. Review
  20. PlGF: a multitasking cytokine with disease-restricted activity.Cold Spring Harbor perspectives in medicine · 2012
    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

8 authors at 1 institution in 1 country.

Pingxi PanLaboratory of Cardiovascular Diseases, National Key Laboratory of Biotherapy of Human Diseases, West China Hospital, Sichuan University, Chengdu, China.
Hua Fu
Lingjun Zhang
He Huang
Fengming Luo
Wenchao Wu
Yingqiang Guo
Xiaojing Liu
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis is now recognized as a chronic inflammatory disease. Angiotensin II (Ang II) is a critical factor in inflammatory responses, which promotes the pathogenesis of atherosclerosis. Placental growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family cytokines and is associated with inflammatory progress of atherosclerosis. However, the potential link between PlGF and Ang II has not been investigated. In the current study, whether Ang II could regulate PlGF expression, and the effect of PlGF on cell proliferation, was investigated in human vascular endothelial cells (VECs) and smooth muscle cells (VSMCs).

resultsIn growth-arrested human VECs and VSMCs, Ang II induced PlGF mRNA expression after 4 hour treatment, and peaked at 24 hours. 10-6 mol/L Ang II increased PlGF protein production after 8 hour treatment, and peaked at 24 hours. Stimulation with Ang II also induced mRNA expression of VEGF receptor-1 and -2(VEGFR-1 and -2) in these cells. The Ang II type I receptor (AT1R) antagonist blocked Ang II-induced PlGF gene expression and protein production. Several intracellular signals elicited by Ang II were involved in PlGF synthesis, including activation of protein kinase C, extracellular signal-regulated kinase 1/2 (ERK1/2) and PI3-kinase. A neutralizing antibody against PlGF partially inhibited the Ang II-induced proliferation of VECs and VSMCs. However, this antibody showed little effect on the basal proliferation in these cells, whereas blocking antibody of VEGF could suppress both basal and Ang II-induced proliferation in VECs and VSMCs.

conclusionOur results showed for the first time that Ang II could induce the gene expression and protein production of PlGF in VECs and VSMCs, which might play an important role in the pathogenesis of vascular inflammation and atherosclerosis.

Indexed as

Angiotensin IIAngiotensin II Type 1 Receptor BlockersAntibodies, BlockingAtherosclerosisCell ProliferationCells, CulturedEndothelium, VascularHumansMitogen-Activated Protein Kinase 3Myocytes, Smooth MusclePhosphatidylinositol 3-KinasesPlacenta Growth FactorPregnancy ProteinsProtein Kinase CSignal TransductionVascular Endothelial Growth Factor Receptor-1Angiotensin IIAngiotensin II Type 1 Receptor BlockersAntibodies, BlockingMitogen-Activated Protein Kinase 3PGF protein, humanPhosphatidylinositol 3-KinasesPlacenta Growth FactorPregnancy ProteinsProtein Kinase CVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID20500895
PMCPMC2885991
OpenAlexW2018919598

What OpenQuestion holds

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LicenceCC BY
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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.