Evidence map›Paper›PMID 30235859›Full record

ArticleCells2018

Platelet-Rich Plasma Prevents In Vitro Transforming Growth Factor-β1-Induced Fibroblast to Myofibroblast Transition: Involvement of Vascular Endothelial Growth Factor (VEGF)-A/VEGF Receptor-1-Mediated Signaling

Flaminia Chellini, Alessia Tani, Larissa Vallone, Daniele Nosi, Paola Pavan, Franco Bambi, Sandra Zecchi Orlandini, Chiara Sassoli

Open access · goldAbstract read
In one paragraph

Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026
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  17. Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism.Frontiers in cell and developmental biology · 2023
    Review
  18. Article
  19. Article
  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

8 authors at 2 institutions in 1 country.

Flaminia ChelliniDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. flaminia.chellini@unifi.it.
Alessia TaniDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. alessia.tani@unifi.it.
Larissa ValloneDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. larissa.vallone@unifi.it.
Daniele NosiDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. daniele.nosi@unifi.it.
Paola PavanTransfusion Medicine and Cell Therapy Unit, "A. Meyer" University Children's Hospital, 50139 Florence, Italy. paola.pavan@meyer.it.
Franco BambiTransfusion Medicine and Cell Therapy Unit, "A. Meyer" University Children's Hospital, 50139 Florence, Italy. franco.bambi@meyer.it.ORCID 0000-0002-1945-8324
Sandra Zecchi OrlandiniDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. sandra.zecchi@unifi.it.
Chiara SassoliDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, 50134 Florence, Italy. chiara.sassoli@unifi.it.ORCID 0000-0002-1337-0938
University of Florence · ITMeyer Children's Hospital · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca ex60% DN, SZO, CS
6 · The paper itself

Abstract

The antifibrotic potential of platelet-rich plasma (PRP) is controversial. This study examined the effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the main drivers of fibrosis, and the involvement of vascular endothelial growth factor (VEGF)-A in mediating PRP-induced responses. The impact of PRP alone on fibroblast differentiation was also assessed. Myofibroblastic phenotype was evaluated by confocal fluorescence microscopy and western blotting analyses of α-smooth muscle actin (sma) and type-1 collagen expression, vinculin-rich focal adhesion clustering, and stress fiber assembly. Notch-1, connexin 43, and VEGF-A expression were also analyzed by RT-PCR. PRP negatively regulated fibroblast-myofibroblast transition via VEGF-A/VEGF receptor (VEGFR)-1-mediated inhibition of TGF-β1/Smad3 signaling. Indeed TGF-β1/PRP co-treated fibroblasts showed a robust attenuation of the myofibroblastic phenotype concomitant with a decrease of Smad3 expression levels. The VEGFR-1 inhibition by KRN633 or blocking antibodies, or VEGF-A neutralization in these cells prevented the PRP-promoted effects. Moreover PRP abrogated the TGF-β1-induced reduction of VEGF-A and VEGFR-1 cell expression. The role of VEGF-A signaling in counteracting myofibroblast generation was confirmed by cell treatment with soluble VEGF-A. PRP as single treatment did not induce fibroblast myodifferentiation. This study provides new insights into cellular and molecular mechanisms underpinning PRP antifibrotic action.

Indexed as

confocal immunofluorescenceConnexin 43fibrosismyofibroblastsNotch-1platelet-rich plasma (PRP)transforming growth factor (TGF)-β1/Smad3vascular endothelial growth factor (VEGF)-AVEGFR-1/flt-1α-smooth muscle actin

Identifiers

PMID30235859
PMCPMC6162453
OpenAlexW2892321210

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.