Evidence map›Paper›PMID 31130964›Full record

ArticleFrontiers in immunology2019

MASP-1 Increases Endothelial Permeability.

Márta L Debreczeni, Zsuzsanna Németh, Erika Kajdácsi, Endre Schwaner, Veronika Makó, András Masszi, Zoltán Doleschall, János Rigó, Fruzsina R Walter, Mária A Deli and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  5. Complement MASP-1 Modifies Endothelial Wound Healing.International journal of molecular sciences · 2024
    Article
  6. Review
  7. Review
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  13. A novel pathogenetic factor of laryngeal attack in hereditary angioedema? Involvement of protease activated receptor 1.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022
    Article
  14. Review
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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

14 authors at 8 institutions in 1 country.

Márta L DebreczeniResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Zsuzsanna NémethResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Erika KajdácsiResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Endre SchwanerResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Veronika MakóMTA-SE Research Group of Immunology and Hematology, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.
András MassziResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Zoltán DoleschallDepartment of Pathogenetics, National Institute of Oncology, Budapest, Hungary.
János RigóFirst Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary.
Fruzsina R WalterBiological Research Centre, Institute of Biophysics, Hungarian Academy of Sciences, Szeged, Hungary.
Mária A DeliBiological Research Centre, Institute of Biophysics, Hungarian Academy of Sciences, Szeged, Hungary.
Gábor PálDepartment of Biochemistry, Eötvös Loránd University, Budapest, Hungary.
József DobóResearch Centre for Natural Sciences, Institute of Enzymology, Hungarian Academy of Sciences, Budapest, Hungary.
Péter GálResearch Centre for Natural Sciences, Institute of Enzymology, Hungarian Academy of Sciences, Budapest, Hungary.
László CervenakResearch Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUEötvös Loránd University · HUHungarian Academy of Sciences · HUHUN-REN Research Centre for Natural Sciences · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUInstitute of Biophysics · HUInstitute of Molecular Life Sciences · HUNational Institute of Oncology · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathologically increased vascular permeability is an important dysfunction in the pathomechanism of life-threatening conditions, such as sepsis, ischemia/reperfusion, or hereditary angioedema (HAE), diseases accompanied by uncontrolled activation of the complement system. HAE for example is caused by the deficiency of C1-inhibitor (the main regulator of early complement activation), which leads to edematous attacks threatening with circulatory collapse. We have previously reported that endothelial cells become activated during HAE attacks. A natural target of C1-inhibitor is mannan-binding lectin-associated serine protease-1 (MASP-1), a multifunctional serine protease, which plays a key role in the activation of complement lectin pathway. We have previously shown that MASP-1 induces the pro-inflammatory activation of endothelial cells and in this study we investigated whether MASP-1 can directly affect endothelial permeability. All experiments were performed on human umbilical vein endothelial cells (HUVECs). Real-time micro electric sensing revealed that MASP-1 decreases the impedance of HUVEC monolayers and in a recently developed permeability test (XperT), MASP-1 dose-dependently increased endothelial paracellular transport. We show that protease activated receptor-1 mediated intracellular Ca

Indexed as

Cells, CulturedHumansHuman Umbilical Vein Endothelial CellsMannose-Binding Protein-Associated Serine ProteasesPermeabilityReceptor, PAR-1Recombinant Proteinsrho-Associated KinasesMannose-Binding Protein-Associated Serine ProteasesMASP1 protein, humanReceptor, PAR-1Recombinant Proteinsrho-Associated KinasesangioedemaC1-inhibitorendothelial cellMASP-1PAR-1permeabilitytranscriptome analysisXPerT assay

Identifiers

PMID31130964
PMCPMC6509239
OpenAlexW2943529840

What Socratic 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 Socratic graph.