Evidence map›Paper›PMID 24204996›Full record

ArticlePloS one2013

Prevention of anti-microbial peptide LL-37-induced apoptosis and ATP release in the urinary bladder by a modified glycosaminoglycan.

Won Yong Lee, Justin R Savage, Jianxing Zhang, Wanjian Jia, Siam Oottamasathien, Glenn D Prestwich

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Epithelial Heparan Sulfate PromotesProteoglycan research · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Prevention of sinonasal inflammation by a synthetic glycosaminoglycan.International forum of allergy & rhinology · 2017
    Article
  16. Bladder pain in an LL-37 interstitial cystitis and painful bladder syndrome model.American journal of clinical and experimental urology · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Won Yong LeeGlycoMira Therapeutics, Inc. Salt Lake City, Utah, United States of America.
Justin R Savage
Jianxing Zhang
Wanjian Jia
Siam Oottamasathien
Glenn D Prestwich
University of Utah · USGlycoMira Therapeutics (United States) · US

Funding

University of Utah Center for Clinical and Translational ScienceUL1TR001067 · NCATS · UNIVERSITY OF UTAH · PI DERE, WILLARD H., HESS, RACHEL · 2013 to 2017
$19.8M
University of Utah Center for clinical and Translational ScienceKL2TR001065 · NCATS · UNIVERSITY OF UTAH · PI DERE, WILLARD H., HESS, RACHEL · 2013 to 2017
$1.1M
Novel Glycosaminoglycan Derivatives for Treatment of Bladder InflammationR43DK093413 · NIDDK · GLYCOMIRA, LLC · PI KENNEDY, THOMAS PRESTON, OOTTAMASATHIEN, SIAM · 2011 to 2011
$200k
NCATS NIH HHS KL2 TR001065NCATS NIH HHS UL1 TR001067NIDDK NIH HHS R43 DK093413NIDDK NIH HHS R43DK093413
6 · The paper itself

Abstract

Interstitial cystitis (IC), often referred to in combination with painful bladder syndrome, is a chronic inflammatory disease of the bladder. Current therapies primarily focus on replenishing urothelial glycosaminoglycan (GAG) layer using GAG analogs and managing pain with supportive therapies. However, the elusive etiology of IC and the lack of animal models to study the disease have been major hurdles developing more effective therapeutics. Previously, we showed an increased urinary concentration of antimicrobial peptide LL-37 in spina bifida patients and used LL-37 to develop a mouse model of cystitis that mimics important clinical findings of IC. Here we investigate (1) the molecular mechanism of LL-37 induced cystitis in cultured human urothelial cells and in mice, (2) the protective effects of GM-0111, a modified GAG, within the context of this mechanism, (3) the physiological and molecular markers that correlate with the severity of the inflammation, and (4) the protective effects of several GAGs using these biomarkers in our LL-37 induced cystitis model. We find that LL-37 quickly induces release of ATP and apoptosis in the urothelium. These changes can be inhibited by a chemically-modified GAG, GM-0111. Furthermore, we also find that GAG analogs provide varying degrees of protection against LL-37 challenge in mice. These findings suggest that GM-0111 and possibly GAG molecules prevent the development of cystitis by blocking the apoptosis and the concurrent release of ATP from the urothelium.

Indexed as

Disease Models, AnimalAdenosine TriphosphateAdjuvants, ImmunologicAnimalsAntimicrobial Cationic PeptidesApoptosisCathelicidinsCystitisFemaleGlycosaminoglycansHumansImmunoenzyme TechniquesInflammationMiceMice, Inbred C57BLUrinary BladderAdenosine TriphosphateAdjuvants, ImmunologicAntimicrobial Cationic PeptidesCathelicidinsGlycosaminoglycans

Identifiers

PMID24204996
PMCPMC3813730
OpenAlexW2054055118

What OpenQuestion holds

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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.