Evidence map›Paper›PMID 19324843›Full record

ArticleInvestigative ophthalmology & visual science2009

Growth factors outside the PDGF family drive experimental PVR.

Hetian Lei, Gisela Velez, Peter Hovland, Tatsuo Hirose, Debra Gilbertson, Andrius Kazlauskas

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Proliferative Vitreoretinopathy: A Reappraisal.Journal of clinical medicine · 2023
    Review
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  7. Article
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  15. Article
  16. Proliferative Vitreoretinopathy: A Review.International ophthalmology clinics · 2019
    Review
  17. Article
  18. Review
  19. Article
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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

6 authors at 4 institutions in 1 country.

Hetian LeiDepartment of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute, Boston, Massachusetts 02114, USA.
Gisela Velez
Peter Hovland
Tatsuo Hirose
Debra Gilbertson
Andrius Kazlauskas
Smith-Kettlewell Eye Research Institute · USHarvard University · USMassachusetts Eye and Ear Infirmary · USRetina Associates · US

Funding

PDGF and PVRR01EY012509 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI LEI, HETIAN · 2000 to 2017
$8.5M
Pharmacologic inhibitors of PDGFR for the treatment of PVRK08EY017383 · NEI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI VELEZ, GISELA · 2007 to 2011
$1.2M
NEI NIH HHS EY012509NEI NIH HHS K08 EY017383NEI NIH HHS R01 EY012509
6 · The paper itself

Abstract

purposeProliferative vitreoretinopathy (PVR) is a recurring and problematic disease for which there is no pharmacologic treatment. Platelet-derived growth factor (PDGF) in the vitreous is associated with experimental and clinical PVR. Furthermore, PDGF receptors (PDGFRs) are present and activated in epiretinal membranes of patient donors, and they are essential for experimental PVR. These observations suggest that PVR arises at least in part from PDGF/PDGFR-driven events. The goal of this study was to determine whether PDGFs were a potential therapeutic target for PVR.

methodsExperimental PVR was induced in rabbits by injecting fibroblasts. Vitreous specimens were collected from experimental rabbits or from patients undergoing vitrectomy to repair retinal detachment. A neutralizing PDGF antibody and a PDGF Trap were tested for their ability to prevent experimental PVR. Activation of PDGFR was monitored by antiphosphotyrosine Western blot analysis of immunoprecipitated PDGFRs. Contraction of collagen gels was monitored in vitro.

resultsNeutralizing vitreal PDGFs did not effectively attenuate PVR, even though the reagents used potently blocked PDGF-dependent activation of the PDGF alpha receptor (PDGFRalpha). Vitreal growth factors outside the PDGF family modestly activated PDGFRalpha and appeared to do so without engaging the ligand-binding domain of PDGFRalpha. This indirect route to activate PDGFRalpha had profound functional consequences. It promoted the contraction of collagen gels and appeared sufficient to drive experimental PVR.

conclusionsAlthough PDGF appears to be a poor therapeutic target, PDGFRalpha is particularly attractive because it can be activated by a much larger spectrum of vitreal growth factors than previously appreciated.

Indexed as

AnimalsAntibodies, MonoclonalBlotting, WesternCell Culture TechniquesCollagen Type IConjunctivaDisease Models, AnimalEpiretinal MembraneFibroblastsHumansIntercellular Signaling Peptides and ProteinsMicePhosphorylationPlatelet-Derived Growth FactorRabbitsReceptor, Platelet-Derived Growth Factor alphaAntibodies, MonoclonalCollagen Type IIntercellular Signaling Peptides and ProteinsPlatelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor alphaRecombinant Fusion ProteinsTyrosine

Identifiers

PMID19324843
PMCPMC2798136
OpenAlexW2117989312

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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.