Evidence map›Paper›PMID 33378942›Full record

ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2021

Alveolar epithelial glycocalyx shedding aggravates the epithelial barrier and disrupts epithelial tight junctions in acute respiratory distress syndrome.

Jun Li, Zhijiang Qi, Dongxiao Li, Xiao Huang, Boyang Qi, Jiali Feng, Jianyu Qu, Xiaozhi Wang

Open access · goldAbstract read
In one paragraph

Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  5. Scutellarein fromPharmaceuticals (Basel, Switzerland) · 2026
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  9. Endothelial glycocalyx glycan expression in lymphatic vasculature in mice.Frontiers in cell and developmental biology · 2026
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  15. Observational
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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

8 authors at 2 institutions in 1 country.

Jun LiSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China; Deparetment of Pulmonary and Critical Care Medicine, Yantai Affiliated Hospital of Binzhou Medical University, YanTai, Shandong, 264100, China.
Zhijiang QiDeparetment of Pulmonary and Critical Care Medicine, Yantai Affiliated Hospital of Binzhou Medical University, YanTai, Shandong, 264100, China.
Dongxiao LiDepartment of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China.
Xiao HuangDepartment of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China.
Boyang QiDepartment of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China.
Jiali FengDepartment of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China.
Jianyu QuDepartment of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China.
Xiaozhi WangSchool of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China; Department of Pulmonary and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou, Shandong, 256603, China. Electronic address: hxicuwxz@163.com.
Binzhou University · CNBinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main pathophysiological mechanism of acute respiratory distress syndrome (ARDS) invovles the increase in alveolar barrier permeability that is primarily caused by epithelial glycocalyx and tight junction (TJ) protein destruction. This study was performed to explore the effects of the alveolar epithelial glycocalyx on the epithelial barrier, specifically on TJ proteins, in ARDS. We used C57BL/6 mice and human lung epithelial cell models of lipopolysaccharide (LPS)-induced ARDS. Changes in alveolar permeability were evaluated via pulmonary histopathology analysis and by measuring the wet/dry weight ratio of the lungs. Degradation of heparan sulfate (HS), an important component of the epithelial glycocalyx, and alterations in levels of the epithelial TJ proteins (occludin, zonula occludens 1, and claudin 4) were assessed via ELISA, immunofluorescence analysis, and western blotting analysis. Real-time quantitative polymerase chain reaction was used to detect the mRNA of the TJ protein. Changes in glycocalyx and TJ ultrastructures in alveolar epithelial cells were evaluated through electron microscopy. In vivo and in vitro, LPS increased the alveolar permeability and led to HS degradation and TJ damage. After LPS stimulation, the expression of the HS-degrading enzyme heparanase (HPA) in the alveolar epithelial cells was increased. The HPA inhibitor N-desulfated/re-N-acetylated heparin alleviated LPS-induced HS degradation and reduced TJ damage. In vitro, recombinant HPA reduced the expression of the TJ protein zonula occludens-1 (ZO-1) and inhibited its mRNA expression in the alveolar epithelial cells. Taken together, our results demonstrate that shedding of the alveolar epithelial glycocalyx aggravates the epithelial barrier and damages epithelial TJ proteins in ARDS, with the underlying mechanism involving the effect of HPA on ZO-1.

Indexed as

A549 CellsAlveolar Epithelial CellsAnimalsBlood-Air BarrierBronchoalveolar Lavage FluidDisease Models, AnimalGlycocalyxHeparan SulfateHumansMaleMiceMice, Inbred C57BLPermeabilityRespiratory Distress SyndromeTight JunctionsZonula Occludens-1 ProteinHeparan SulfateTJP1 protein, humanZonula Occludens-1 ProteinAcute respiratory distress syndromeAlveolar barrierAlveolar epithelial glycocalyxHeparanaseTight junction proteins

Identifiers

PMID33378942
PMCPMC7685063
OpenAlexW3108436615

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.