Evidence map›Paper›PMID 22745308›Full record

ArticleDevelopment (Cambridge, England)2012

Glycosaminoglycan-dependent restriction of FGF diffusion is necessary for lacrimal gland development.

Xiuxia Qu, Yi Pan, Christian Carbe, Andrea Powers, Kay Grobe, Xin Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-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

35 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Heparin is essential for optimal cell signaling by FGF21 and for regulation of βKlotho cellular stability.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Review
  4. Review
  5. Article
  6. Lacrimal gland choristomas.Arquivos brasileiros de oftalmologia · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Lacrimal gland development: From signaling interactions to regenerative medicine.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The role of heparan sulphate in development: the ectodermal story.International journal of experimental pathology · 2016
    Review
  18. Mechanisms of FGF gradient formation during embryogenesis.Seminars in cell & developmental biology · 2016
    Review
  19. 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

6 authors at 4 institutions in 3 countries.

Xiuxia QuDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Yi Pan
Christian Carbe
Andrea Powers
Kay Grobe
Xin Zhang
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineChinese Academy of Sciences · CNUniversity of Münster · DE

Funding

Regulation of FGF signaling in lacrimal gland developmentR01EY018868 · NEI · INDIANA UNIVERSITY INDIANAPOLIS · PI Xin Zhang · 2009 to 2026
$6.3M
NEI NIH HHS EY018868NEI NIH HHS R01 EY018868
6 · The paper itself

Abstract

Glycosaminoglycans (GAGs) play a central role in embryonic development by regulating the movement and signaling of morphogens. We have previously demonstrated that GAGs are the co-receptors for Fgf10 signaling in the lacrimal gland epithelium, but their function in the Fgf10-producing periocular mesenchyme is still poorly understood. In this study, we have generated a mesenchymal ablation of UDP-glucose dehydrogenase (Ugdh), an essential biosynthetic enzyme for GAGs. Although Fgf10 RNA is expressed normally in the periocular mesenchyme, Ugdh mutation leads to excessive dispersion of Fgf10 protein, which fails to elicit an FGF signaling response or budding morphogenesis in the presumptive lacrimal gland epithelium. This is supported by genetic rescue experiments in which the Ugdh lacrimal gland defect is ameliorated by constitutive Ras activation in the epithelium but not in the mesenchyme. We further show that lacrimal gland development requires the mesenchymal expression of the heparan sulfate N-sulfation genes Ndst1 and Ndst2 but not the 6-O and 2-O-sulfation genes Hs6st1, Hs6st2 and Hs2st. Taken together, these results demonstrate that mesenchymal GAG controls lacrimal gland induction by restricting the diffusion of Fgf10.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCrosses, GeneticDiffusionFibroblast Growth Factor 10Fibroblast Growth FactorsGenomicsGlycosaminoglycansHeparan SulfateLacrimal ApparatusLigandsMiceMice, Inbred C57BLModels, BiologicalModels, GeneticSignal TransductionFgf10 protein, mouseFibroblast Growth Factor 10Fibroblast Growth FactorsGlycosaminoglycansHeparan SulfateLigandsUridine Diphosphate Glucose Dehydrogenase

Identifiers

PMID22745308
PMCPMC3392702
OpenAlexW2103077266

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.