Evidence map›Paper›PMID 29856065›Full record

ArticleJournal of cellular physiology2018

Isoform-specific effects of transforming growth factor β on endothelial-to-mesenchymal transition.

Harika Sabbineni, Arti Verma, Payaningal R Somanath

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  17. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.International journal of molecular sciences · 2024
    Review
  18. Review
  19. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  20. Article
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

3 authors at 1 institution in 1 country.

Harika SabbineniDepartment of Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia.
Arti VermaDepartment of Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia.
Payaningal R SomanathDepartment of Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia.ORCID 0000-0003-3017-0230
University of Georgia · US

Funding

Protein kinase B (Akt)-mediated pathway regulating endothelial-barrier functionR01HL103952 · NHLBI · UNIVERSITY OF GEORGIA · PI SHENOY, SOMANATH P RAMMOHAN · 2011 to 2015
$1.5M
NHLBI NIH HHS R01 HL103952
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) was first reported in the embryogenesis. Recent studies show that EndMT also occurs in the disease progression of atherosclerosis, cardiac and pulmonary fibrosis, pulmonary hypertension, diabetic nephropathy, and cancer. Although transforming growth factor β (TGFβ) is crucial for EndMT, it is not clear which isoform elicits a predominant effect. The current study aims to directly compare the dose-dependent effects of TGFβ1, TGFβ2, and TGFβ3 on EndMT and characterize the underlying mechanisms. In our results, all three TGFβ isoforms induced EndMT in human microvascular endothelial cells after 72 hr, as evidenced by the increased expression of mesenchymal markers N-cadherin and α-smooth muscle actin as well as the decreased expression of endothelial nitric oxide synthase. Interestingly, the effect of TGFβ2 was the most pronounced. At 1 ng/ml, only TGFβ2 treatment resulted in significantly increased phosphorylation (activation) of Smad2/3 and p38-MAPK and increased expression of mesenchymal transcription factors Snail and FoxC2. Intriguingly, we observed that treatment with 1 ng/ml TGFβ1 and TGFβ3, but not TGFβ2, resulted in an increased expression of TGFβ2, thus indicating that EndMT with TGFβ1 and TGFβ3 treatments was due to the secondary effects through TGFβ2 secretion. Furthermore, silencing TGFβ2 using small interfering RNA blunted the expression of EndMT markers in TGFβ1- and TGFβ3-treated cells. Together, our results indicate that TGFβ2 is the most potent inducer of EndMT and that TGFβ1- and TGFβ3-induced EndMT necessitates a paracrine loop involving TGFβ2.

Indexed as

AtherosclerosisCadherinsDiabetic NephropathiesEndothelial CellsForkhead Transcription FactorsGene Expression RegulationHumansHypertension, PulmonaryMesodermNeoplasmsp38 Mitogen-Activated Protein KinasesParacrine CommunicationProtein IsoformsRNA, Small InterferingSmad2 ProteinSnail Family Transcription FactorsCadherinsForkhead Transcription Factorsmesenchyme fork head 1 proteinp38 Mitogen-Activated Protein KinasesProtein IsoformsRNA, Small InterferingSmad2 ProteinSMAD2 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTGFB1 protein, humanTGFB2 protein, humanTGFB3 protein, humanTransforming Growth Factor beta1Transforming Growth Factor beta2Transforming Growth Factor beta3EndMTFoxC2N-cadherinSnailTGFβ1TGFβ2TGFβ3

Identifiers

PMID29856065
PMCPMC6415927
OpenAlexW2805927967

What OpenQuestion holds

Textmetadata
LicenceTDM
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.