Evidence map›Paper›PMID 30760748›Full record

ArticleScientific reports2019

Expression, activity and localization of lysosomal sulfatases in Chronic Obstructive Pulmonary Disease.

Julie Weidner, Prajakta Jogdand, Linnea Jarenbäck, Ida Åberg, Dalja Helihel, Jaro Ankerst, Gunilla Westergren-Thorsson, Leif Bjermer, Jonas S Erjefält, Ellen Tufvesson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Mucins 3A and 3B Are Expressed in the Epithelium of Human Large Airway.International journal of molecular sciences · 2023
    Observational
  4. Article
  5. Article
  6. Sex Hormones and Lung Inflammation.Advances in experimental medicine and biology · 2021
    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

10 authors at 1 institution in 1 country.

Julie WeidnerRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Prajakta JogdandAirway Inflammation, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Linnea JarenbäckRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Ida ÅbergRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Dalja HelihelRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Jaro AnkerstRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Gunilla Westergren-ThorssonLung Biology, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Leif BjermerRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Jonas S ErjefältAirway Inflammation, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Ellen TufvessonRespiratory Medicine and Allergology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden. ellen.tufvesson@med.lu.se.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a leading cause of death world-wide. Recently, we showed that COPD is associated with gene polymorphisms in SUMF1, a master regulator of sulfatases. Sulfatases are involved in extracellular matrix remodeling and activated by SUMF1, but their role in the lung is poorly described. We aimed to examine how sulfatases are affected in the airways of patients with COPD compared to ever smokers and never smokers. We observed that mRNA expression of the sulfatases GALNS, GNS and IDS was increased, while protein expression of many sulfatases was decreased in COPD fibroblasts. Several sulfatases, including GALNS, IDS, and SGSH, showed increased activity in COPD fibroblasts. Examination of different sulfatases by immunofluorescence showed that IDS, ARSB, GNS and SGSH in fibroblasts were localized to sites other than their reported destination. Using a master panel from different organs, RNA expression of all sulfatases could be observed in lung tissue. Additionally, immunohistochemistry on lung biopsies indicated differing expression of sulfatases in COPD patients. In conclusion, mRNA, protein expression, sulfatase activity levels, and localization of sulfatases are altered in lung fibroblasts and lung tissue from COPD patients and may be mechanistically important in COPD pathogenesis. This could contribute to the understanding of the disease mechanism in COPD and in the long run, to lead to more individualized therapies.

Indexed as

ChondroitinsulfatasesFemaleGlycoproteinsHumansHydrolasesLungMaleOxidoreductases Acting on Sulfur Group DonorsPulmonary Disease, Chronic ObstructiveRNA, MessengerSmokersSulfatasesChondroitinsulfatasesGALNS protein, humanGlycoproteinsHydrolasesIDS protein, humanN-sulfoglucosamine sulfohydrolaseOxidoreductases Acting on Sulfur Group DonorsRNA, MessengerSulfatasesSUMF1 protein, human

Identifiers

PMID30760748
PMCPMC6374378
OpenAlexW2921333489

What OpenQuestion holds

Textmetadata
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.