Evidence map›Paper›PMID 29529029›Full record

ArticlePLoS genetics2018

Müller glia-derived PRSS56 is required to sustain ocular axial growth and prevent refractive error.

Seyyedhassan Paylakhi, Cassandre Labelle-Dumais, Nicholas G Tolman, Michael A Sellarole, Yusef Seymens, Joseph Saunders, Hesham Lakosha, Wilhelmine N deVries, Andrew C Orr, Piotr Topilko and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Insights into Myopia from Mouse Models.Annual review of vision science · 2024
    Review
  12. Article
  13. Cell-cell interaction in the pathogenesis of inherited retinal diseases.Frontiers in cell and developmental biology · 2024
    Review
  14. Retinal glia in myopia: current understanding and future directions.Frontiers in cell and developmental biology · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Role of Retinal Dysfunction in Myopia Development.Cellular and molecular neurobiology · 2023
    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

12 authors at 5 institutions in 3 countries.

Seyyedhassan PaylakhiDepartment of Ophthalmology, University of California, San Francisco, California, United States of America.
Cassandre Labelle-DumaisDepartment of Ophthalmology, University of California, San Francisco, California, United States of America.
Nicholas G TolmanHoward Hughes Medical Institute, The Jackson Laboratory, Bar Harbor, ME, United States of America.
Michael A SellaroleDepartment of Ophthalmology, University of California, San Francisco, California, United States of America.
Yusef SeymensDepartment of Ophthalmology, University of California, San Francisco, California, United States of America.ORCID 0000-0002-3778-4078
Joseph SaundersDepartment of Ophthalmology and Visual Sciences, Dalhousie University, Halifax, NS, Canada.
Hesham LakoshaDepartment of Ophthalmology and Visual Sciences, Dalhousie University, Halifax, NS, Canada.
Wilhelmine N deVriesHoward Hughes Medical Institute, The Jackson Laboratory, Bar Harbor, ME, United States of America.ORCID 0000-0001-8229-9357
Andrew C OrrDepartment of Ophthalmology and Visual Sciences, Dalhousie University, Halifax, NS, Canada.ORCID 0000-0002-9388-9034
Piotr TopilkoEcole Normale Supérieure, Institut de Biologie de l'ENS (IBENS), and Inserm U1024, and CNRS UMR 8197, Paris, France.
Simon Wm JohnHoward Hughes Medical Institute, The Jackson Laboratory, Bar Harbor, ME, United States of America.
K Saidas NairDepartment of Ophthalmology, University of California, San Francisco, California, United States of America.ORCID 0000-0001-5309-9727
University of California, San Francisco · USDalhousie University · CAHoward Hughes Medical Institute · USCentre National de la Recherche Scientifique · FRTufts University · US

Funding

Rapid-Prototyping and Design CoreP30EY002162 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LAMBA, DEEPAK ASHOK · 1985 to 2024
$16.8M
Factors Determining Intraocular Pressure and Glaucoma SusceptibilityR01EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 2002 to 2018
$12.4M
Determining Molecular and Cellular Mechanisms of GlaucomaR01EY022891 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NAIR, KAYARAT SAIDAS · 2013 to 2017
$2.0M
FACTORS DETERMINING INTRAOCULAR PRESSURER29EY011721 · NEI · JACKSON LABORATORY · PI JOHN, SIMON W · 1997 to 2001
$227k
NEI NIH HHS P30 EY002162NEI NIH HHS R01 EY011721NEI NIH HHS R01 EY022891NEI NIH HHS R29 EY011721NIH HHS EY011721
6 · The paper itself

Abstract

A mismatch between optical power and ocular axial length results in refractive errors. Uncorrected refractive errors constitute the most common cause of vision loss and second leading cause of blindness worldwide. Although the retina is known to play a critical role in regulating ocular growth and refractive development, the precise factors and mechanisms involved are poorly defined. We have previously identified a role for the secreted serine protease PRSS56 in ocular size determination and PRSS56 variants have been implicated in the etiology of both hyperopia and myopia, highlighting its importance in refractive development. Here, we use a combination of genetic mouse models to demonstrate that Prss56 mutations leading to reduced ocular size and hyperopia act via a loss of function mechanism. Using a conditional gene targeting strategy, we show that PRSS56 derived from Müller glia contributes to ocular growth, implicating a new retinal cell type in ocular size determination. Importantly, we demonstrate that persistent activity of PRSS56 is required during distinct developmental stages spanning the pre- and post-eye opening periods to ensure optimal ocular growth. Thus, our mouse data provide evidence for the existence of a molecule contributing to both the prenatal and postnatal stages of human ocular growth. Finally, we demonstrate that genetic inactivation of Prss56 rescues axial elongation in a mouse model of myopia caused by a null mutation in Egr1. Overall, our findings identify PRSS56 as a potential therapeutic target for modulating ocular growth aimed at preventing or slowing down myopia, which is reaching epidemic proportions.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsDisease Models, AnimalEarly Growth Response Protein 1EyeFemaleHumansHyperopiaMaleMice, Mutant StrainsMice, TransgenicMyopiaNeurogliaRefraction, OcularRefractive ErrorsSerine ProteasesEarly Growth Response Protein 1Egr1 protein, mousePRSS56 protein, humanPrss56 protein, mouseSerine Proteases

Identifiers

PMID29529029
PMCPMC5864079
OpenAlexW2790975139

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.