Evidence map›Paper›PMID 22889846›Full record

ArticleThe American journal of pathology2012

A RHAMM mimetic peptide blocks hyaluronan signaling and reduces inflammation and fibrogenesis in excisional skin wounds.

Cornelia Tolg, Sara R Hamilton, Ewa Zalinska, Lori McCulloch, Ripal Amin, Natalia Akentieva, Francoise Winnik, Rashmin Savani, Darius J Bagli, Len G Luyt and 3 more

Abstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

78 citing papers in PubMed, 121 citations in OpenAlex.

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  12. Evaluation of Extracellular Matrix Remodeling in Full-thickness Skin Grafts in Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
    Article
  13. Article
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  15. Article
  16. Article
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  18. Review
  19. "Annals of pancreatic cancer · 2022
    Article
  20. Methods for isolating and analyzing physiological hyaluronan: a review.American journal of physiology. Cell physiology · 2022
    Review

18 more citing papers are in PubMed but not listed here.

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

13 authors at 9 institutions in 2 countries.

Cornelia TolgCancer Research Laboratory Program, Lawson Health Research Institute and London Regional Cancer Program, London Health Sciences Center, London, Ontario, Canada.
Sara R Hamilton
Ewa Zalinska
Lori McCulloch
Ripal Amin
Natalia Akentieva
Francoise Winnik
Rashmin Savani
Darius J Bagli
Len G Luyt
Mary K Cowman
Jim B McCarthy
Eva A Turley
Lawson Health Research Institute · CAHospital for Sick Children · CAWestern University · CANew York University · USSUNY Polytechnic Institute · USThe University of Texas Southwestern Medical Center · USUniversité de Montréal · CAUniversity of Minnesota · USUniversity of Toronto · CA

Funding

Hyaluronan Receptors in Prostate Cancer ProgressionR01CA119092 · NCI · UNIVERSITY OF MINNESOTA · PI MCCARTHY, JAMES B. · 2008 to 2012
$2.2M
NCI NIH HHS 5R01CA119092NCI NIH HHS R01 CA119092
6 · The paper itself

Abstract

Hyaluronan is activated by fragmentation and controls inflammation and fibroplasia during wound repair and diseases (eg, cancer). Hyaluronan-binding peptides were identified that modify fibrogenesis during skin wound repair. Peptides were selected from 7- to 15mer phage display libraries by panning with hyaluronan-Sepharose beads and assayed for their ability to block fibroblast migration in response to hyaluronan oligosaccharides (10 kDa). A 15mer peptide (P15-1), with homology to receptor for hyaluronan mediated motility (RHAMM) hyaluronan binding sequences, was the most effective inhibitor. P15-1 bound to 10-kDa hyaluronan with an affinity of K(d) = 10(-7) and appeared to specifically mimic RHAMM since it significantly reduced binding of hyaluronan oligosaccharides to recombinant RHAMM but not to recombinant CD44 or TLR2,4, and altered wound repair in wild-type but not RHAMM(-/-) mice. One topical application of P15-1 to full-thickness excisional rat wounds significantly reduced wound macrophage number, fibroblast number, and blood vessel density compared to scrambled, negative control peptides. Wound collagen 1, transforming growth factor β-1, and α-smooth muscle actin were reduced, whereas tenascin C was increased, suggesting that P15-1 promoted a form of scarless healing. Signaling/microarray analyses showed that P15-1 blocks RHAMM-regulated focal adhesion kinase pathways in fibroblasts. These results identify a new class of reagents that attenuate proinflammatory, fibrotic repair by blocking hyaluronan oligosaccharide signaling.

Indexed as

AnimalsBinding, CompetitiveCell CountCell DifferentiationCell MovementCollagenExtracellular Matrix ProteinsFemaleFibroblastsFibrosisHumansHyaluronan ReceptorsHyaluronic AcidInflammationMacrophagesMiceCollagenExtracellular Matrix Proteinshyaluronan-mediated motility receptorHyaluronan ReceptorsHyaluronic AcidPeptidesRecombinant ProteinsTenascinTransforming Growth Factor beta1

Identifiers

PMID22889846
PMCPMC3463631
OpenAlexW2015472266

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.