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Related Experiment Video

Updated: Mar 14, 2026

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Procalcitonin Impairs Endothelial Cell Function and Viability.

Nana-Maria Wagner1, Caroline Van Aken, Antje Butschkau

  • 1From the *Department of Anesthesiology and Critical Care Medicine and †Institute for Experimental Surgery, University Hospital Rostock, Rostock, Germany; ‡Department of Anesthesiology and Intensive Care, University of Luebeck, University Medical Center Schleswig-Holstein, Luebeck, Germany; §Molecular and Experimental Mycobacteriology, Research Center Borstel, Germany; and ‖Institute of Human Genetics, University Hospital Muenster, Muenster, Germany.

Anesthesia and Analgesia
|September 23, 2016
PubMed
Summary
This summary is machine-generated.

Procalcitonin, a sepsis biomarker, impairs endothelial cell function, reducing barrier integrity and new vessel formation. This suggests procalcitonin may contribute to sepsis-induced hypotension and vascular disease.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathophysiology

Background:

  • Procalcitonin (PCT) is a biomarker for sepsis severity and risk stratification.
  • Endothelial cell dysfunction is critical in sepsis pathogenesis, leading to hypotension and organ hypoperfusion.
  • The direct effects of PCT on endothelial cells remain largely unexplored.

Purpose of the Study:

  • To investigate the direct impact of procalcitonin on endothelial cell function and viability.
  • To determine if PCT influences endothelial barrier integrity, migration, and angiogenesis.
  • To assess PCT's role in endothelial response to ischemic conditions.

Main Methods:

  • Human endothelial cells were exposed to varying PCT concentrations (0.01–100 ng/mL) in vitro.
  • Assays included transwell permeability, scratch wound migration, and capillary formation.
  • In vivo studies used a murine model of hindlimb ischemia; molecular analyses involved immunoblotting, flow cytometry, and genomic analysis.

Main Results:

  • PCT induced endothelial barrier disruption and reduced cell migration and in vitro angiogenesis.
  • In vivo, PCT impaired neovascularization and hindlimb perfusion recovery post-ischemia.
  • PCT decreased vascular endothelial-cadherin expression and induced endothelial cell apoptosis at higher concentrations.

Conclusions:

  • Procalcitonin directly impairs endothelial cell function, including barrier integrity and angiogenesis.
  • PCT-induced endothelial dysfunction may contribute to sepsis-related hypotension and vascular complications.
  • Further research into PCT as a therapeutic target for vascular dysfunction in inflammatory conditions is warranted.