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MASP-1 Increases Endothelial Permeability.

Márta L Debreczeni1, Zsuzsanna Németh1, Erika Kajdácsi1

  • 1Research Laboratory, 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.

Frontiers in Immunology
|May 28, 2019
PubMed
Summary
This summary is machine-generated.

Mannan-binding lectin-associated serine protease-1 (MASP-1) increases vascular permeability by affecting endothelial cells. This finding may lead to new anti-edema drug development for conditions like hereditary angioedema.

Keywords:
C1-inhibitorMASP-1PAR-1XPerT assayangioedemaendothelial cellpermeabilitytranscriptome analysis

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Area of Science:

  • Immunology
  • Vascular Biology
  • Biochemistry

Background:

  • Pathologically increased vascular permeability contributes to severe conditions like sepsis and hereditary angioedema (HAE).
  • HAE involves C1-inhibitor deficiency, leading to uncontrolled complement activation and dangerous edema.
  • Mannan-binding lectin-associated serine protease-1 (MASP-1) is a key enzyme in complement lectin pathway activation.

Purpose of the Study:

  • To investigate the direct effect of MASP-1 on endothelial permeability.
  • To elucidate the molecular mechanisms by which MASP-1 influences endothelial barrier function.

Main Methods:

  • Experiments conducted on human umbilical vein endothelial cells (HUVECs).
  • Real-time micro electric sensing to measure endothelial cell impedance.
  • XperT permeability assay to assess paracellular transport.
  • Analysis of intracellular signaling pathways (Ca2+, Rho-kinase, MLC phosphorylation).
  • Whole-transcriptome microarray analysis to identify gene expression changes.

Main Results:

  • MASP-1 significantly decreased HUVEC monolayer impedance.
  • MASP-1 dose-dependently increased endothelial paracellular transport.
  • MASP-1 induced intracellular Ca2+ mobilization, Rho-kinase activation, and cytoskeletal changes.
  • MASP-1 altered the expression of 25 permeability-related genes, including upregulation of the bradykinin B2 receptor.

Conclusions:

  • MASP-1 directly increases endothelial permeability through specific molecular pathways.
  • MASP-1 may contribute to edema in diseases with complement activation.
  • MASP-1 represents a potential therapeutic target for anti-edema drug development.