Evidence map›Paper›PMID 20554532›Full record

ArticleThe Journal of biological chemistry2010

Reactive oxygen species and hyaluronidase 2 regulate airway epithelial hyaluronan fragmentation.

Maria E Monzon, Nevis Fregien, Nathalie Schmid, Nieves S Falcon, Michael Campos, S Marina Casalino-Matsuda, Rosanna Malbran Forteza

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed, 108 citations in OpenAlex.

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  11. Proteoglycans in Toll-like receptor responses and innate immunity.American journal of physiology. Cell physiology · 2022
    Review
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  14. Article
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  16. Hyaluronan and Its Receptors as Regulatory Molecules of the Endothelial Interface.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  17. Review
  18. Article
  19. Expression and activity of hyaluronidases HYAL-1, HYAL-2 and HYAL-3 in the human intervertebral disc.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2020
    Article
  20. Article

1 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

7 authors at 1 institution in 1 country.

Maria E MonzonDivision of Pulmonary Critical Care Sleep Medicine, University of Miami, Miller School of Medicine, Miami, Florida 33136, USA. mmonzonmedina@med.miami.edu
Nevis Fregien
Nathalie Schmid
Nieves S Falcon
Michael Campos
S Marina Casalino-Matsuda
Rosanna Malbran Forteza
University of Miami · US

Funding

MECHANISMS OF OXIDANT-INDUCED CHRONIC BRONCHITISR01HL073156 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MALBRAN FORTEZA, ROSANNA C · 2003 to 2012
$2.8M
NHLBI NIH HHS HL-073156NHLBI NIH HHS R01 HL073156
6 · The paper itself

Abstract

Hyaluronidase 2 (Hyal2) is a hyaluronan (HA)-degrading enzyme found intracellularly or/and anchored to the plasma membrane through glycosylphosphatidylinositol (GPI). Normal human bronchial epithelial cells (NHBE) grown at the air-liquid interphase (ALI), treated with PI-specific phospholipase C (PI-PLC), exhibited increased Hyal activity in secretions and decreased protein and activity on the apical membrane, confirming that GPI-anchored Hyal2 is expressed in NHBE cells and it remains active in its soluble form. We have reported that HA degradation was mediated by reactive oxygen species (ROS) in human airways. Here we show that ROS increase Hyal2 expression and activity in NHBE cells and that the p38MAPK signaling pathway is involved in this effect. Hyal2 induction was confirmed by using small interfering RNA (siRNA) expressing lentivirus. These in vitro findings correlated in vivo with smokers, where increased Hyal2 immunoreactivity in the epithelium was associated with augmented levels of HA and the appearance of low molecular mass HA species in bronchial secretions. In summary, this work provides evidence that ROS induce Hyal2, suggesting that Hyal2 is likely responsible for the sustained HA fragmentation in the airway lumen observed in inflammatory conditions associated with oxidative stress.

Indexed as

Antigens, NeoplasmCells, CulturedGlycosylphosphatidylinositolsHistone AcetyltransferasesHumansHyaluronic AcidHyaluronoglucosaminidaseInflammationMAP Kinase Signaling SystemOxidative StressReactive Oxygen SpeciesRespiratory MucosaAntigens, NeoplasmGlycosylphosphatidylinositolsHistone AcetyltransferasesHyaluronic AcidHyaluronoglucosaminidaseOGA protein, humanReactive Oxygen Species

Identifiers

PMID20554532
PMCPMC2924017
OpenAlexW2137630610

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.