Evidence map›Paper›PMID 21257926›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

Hyaluronan fragments promote inflammation by down-regulating the anti-inflammatory A2a receptor.

Samuel L Collins, Katharine E Black, Yee Chan-Li, Young-Hoon Ahn, Philip A Cole, Jonathan D Powell, Maureen R Horton

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Effect of hyaluronic acid on radiotherapy-induced mucocutaneous side effects: a meta-analysis of randomized controlled trials.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022
    Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Prostaglandin EBiology · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Cell Energy Metabolism and Hyaluronan Synthesis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Activation of AAmerican journal of translational research · 2017
    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

7 authors at 1 institution in 1 country.

Samuel L CollinsDepartment of Medicine, Division of Pulmonary and Critical Care, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Katharine E Black
Yee Chan-Li
Young-Hoon Ahn
Philip A Cole
Jonathan D Powell
Maureen R Horton
Johns Hopkins University · US

Funding

Hyaluronan-Induced Signaling and Gene RegulationR01HL073855 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HORTON, MAUREEN RENEE · 2003 to 2010
$1.9M
The A2a adenosine receptor modulates hyaluronan mediated lung inflammationR01HL086632 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HORTON, MAUREEN RENEE · 2007 to 2010
$1.5M
NHLBI NIH HHS R01 HL073855NHLBI NIH HHS R01 HL086632NHLBI NIH HHS R01 HL0866332
6 · The paper itself

Abstract

The tissue microenvironment plays a critical role in regulating inflammation. Chronic inflammation leads to an influx of inflammatory cells and mediators, extracellular matrix turnover, and increased extracellular adenosine. Low molecular weight (LMW) fragments of hyaluronan (HA), a matrix component, play a critical role in lung inflammation and fibrosis by inducing inflammatory gene expression at the injury site. Adenosine, a crucial negative regulator of inflammation, protects tissues from immune destruction via the adenosine A2a receptor (A2aR). Therefore, these two extracellular products of inflammation play opposing roles in regulating immune responses. As such, we wanted to determine the effect of LMW HA on A2aR function. In this article, we demonstrate that LMW HA causes a rapid, significant, and sustained down-regulation of the A2aR. CD44 was found to be necessary for LMW HA to down-modulate the A2aR as was protein kinase C signaling. We also demonstrate that LMW HA induces A2aR down-regulation during inflammation in vivo, and that this down-regulation can be blocked by treatment with an HA-blocking peptide. Because adenosine plays a critical role in limiting inflammation, our data provide a novel mechanism whereby LMW HA itself may further augment inflammation. By defining the pro- and anti-inflammatory properties of extracellular matrix components, we will be better able to identify specific pharmacologic targets as potential therapies.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineDisease Models, AnimalDown-RegulationHyaluronan ReceptorsHyaluronic AcidInflammation MediatorsLipopolysaccharidesMacrophages, AlveolarMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Peptide FragmentsAnti-Inflammatory AgentsCd44 protein, mouseHyaluronan ReceptorsHyaluronic AcidInflammation MediatorsLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88Peptide FragmentsPeptidesProtein Kinase CProtein Kinase InhibitorsReceptor, Adenosine A2ARNA, MessengerTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID21257926
PMCPMC3208614
OpenAlexW2060542943

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.