Evidence map›Paper›PMID 33705750›Full record

ArticleThe American journal of pathology2021

The Canonical Wnt Signaling Pathway Inhibits the Glucocorticoid Receptor Signaling Pathway in the Trabecular Meshwork.

Chenna Kesavulu Sugali, Naga Pradeep Rayana, Jiannong Dai, Michael Peng, Sherri L Harris, Hannah C Webber, Shaohui Liu, Stephan G Dixon, Priyanka H Parekh, Elizabeth A Martin and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. GSK3β Inhibitors Inhibit TGFβ Signaling in the Human Trabecular Meshwork.Investigative ophthalmology & visual science · 2024
    Article
  7. Article
  8. Glucocorticoid-Induced Ocular Hypertension and Glaucoma.Clinical ophthalmology (Auckland, N.Z.) · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023
    Review
  13. Article
  14. iPSCs-Based Therapy for Trabecular Meshwork.Handbook of experimental pharmacology · 2023
    Article
  15. Viral Vector-Induced Ocular Hypertension in Mice.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  16. International journal of ophthalmology · 2023
    Article
  17. Article
  18. Article
  19. 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

20 authors at 3 institutions in 1 country.

Chenna Kesavulu SugaliDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Naga Pradeep RayanaDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Jiannong DaiDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Michael PengDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Sherri L HarrisDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas.
Hannah C WebberDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas.
Shaohui LiuDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Stephan G DixonDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Priyanka H ParekhDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Elizabeth A MartinDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Louis B CantorDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana.
Ronald L FellmanDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
David G GodfreyDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
Michelle R ButlerDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
Matthew E EmanuelDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
Davinder S GroverDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
Oluwatosin U SmithDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas; Glaucoma Associates of Texas, Dallas, Texas.
Abbot F ClarkDepartment of Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas.
Vijay Krishna RaghunathanDepartment of Basic Sciences, College of Optometry, University of Houston, Houston, Texas.
Weiming MaoDepartment of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: weimmao@iu.edu.
Indiana University School of MedicineUniversity of North Texas · USUniversity of Houston · US

Funding

Quality Assurance and Quality Control Project Management: Improving Submissions and Study Conduct in the Human Subjects Research Prior Approval ProcessUL1TR002529 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M, WIEHE, SARAH ELIZABETH · 2018 to 2022
$27.2M
Glucocorticoids, ocular hypertension and glaucomaR01EY030967 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI CLARK, ABBOT FREDERICK, GEISERT, ELDON E · 2020 to 2024
$2.8M
Cross-talk between TGF-beta and Wnt pathways in the trabecular meshworkR01EY026962 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI MAO, WEIMING · 2017 to 2021
$1.9M
Mechanotransduction in Aqueous Outflow Regulation and Open Angle GlaucomaR01EY026048 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ACOTT, TED S, RAGHUNATHAN, VIJAYKRISHNA · 2018 to 2021
$1.5M
NCATS NIH HHS UL1 TR002529NEI NIH HHS R01 EY026048NEI NIH HHS R01 EY026962NEI NIH HHS R01 EY030967
6 · The paper itself

Abstract

Glucocorticoid-induced glaucoma is a secondary open-angle glaucoma. About 40% of the general population may develop elevated intraocular pressure on prolonged glucocorticoid treatment secondary to damages in the trabecular meshwork (TM), a tissue that regulates intraocular pressure. Therefore, identifying the key molecules responsible for glucocorticoid-induced ocular hypertension is crucial. In this study, Dickkopf-related protein 1 (Dkk1), a canonical Wnt signaling inhibitor, was found to be elevated in the aqueous humor and TM of glaucoma patients. At the signaling level, Dkk1 enhanced glucocorticoid receptor (GR) signaling, whereas Dkk1 knockdown or Wnt signaling activators decreased GR signaling in human TM cells as indicated by luciferase assays. Similarly, activation of the GR signaling inhibited Wnt signaling. At the protein level, glucocorticoid-induced extracellular matrix was inhibited by Wnt activation using Wnt activators or Dkk1 knockdown in primary human TM cells. In contrast, inhibition of canonical Wnt signaling by β-catenin knockdown increased glucocorticoid-induced extracellular matrix proteins. At the physiological level, adenovirus-mediated Wnt3a expression decreased glucocorticoid-induced ocular hypertension in mouse eyes. In summary, Wnt and GR signaling inhibit each other in the TM, and canonical Wnt signaling activators may prevent the adverse effect of glucocorticoids in the eye.

Indexed as

AnimalsFemaleGlaucomaGlucocorticoidsHumansImmunosuppressive AgentsMiceMice, Inbred C57BLReceptors, GlucocorticoidTrabecular MeshworkWnt Signaling PathwayGlucocorticoidsImmunosuppressive AgentsReceptors, Glucocorticoid

Identifiers

PMID33705750
PMCPMC8176142
OpenAlexW3134848994

What OpenQuestion holds

Textmetadata
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.