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Procalcitonin mediates vascular dysfunction in obesity.

Laura Brabenec1, Katharina E M Hellenthal1, Melanie Müller1

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Obesity-related inflammation involves procalcitonin (PCT) from fat tissue impairing blood vessel function. Blocking PCT signaling may improve endothelial health in obese individuals.

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Area of Science:

  • Endocrinology
  • Vascular Biology
  • Inflammation Research

Background:

  • Obesity is linked to chronic inflammation, endothelial dysfunction, and vascular issues.
  • Procalcitonin (PCT), an inflammation marker secreted by adipose tissue, is elevated in obesity.

Purpose of the Study:

  • To investigate if visceral or perivascular fat-derived PCT contributes to obesity-induced endothelial dysfunction.
  • To explore PCT as a potential therapeutic target for improving vascular health in obesity.

Main Methods:

  • Western blot for PCT expression in adipose tissues.
  • Murine endothelial cell assays for reactive oxygen species (ROS) and nitric oxide (NO) production.
  • Ex vivo analysis of endothelium-dependent vasorelaxation in murine arterioles using pressure myography.
  • Pharmacological manipulation using calcitonin gene-related peptide (CGRP), CRLR/RAMP1 antagonist olcegepant, and DPP4 inhibitor sitagliptin.

Main Results:

  • PCT was found in visceral, perivascular, and epicardial adipose tissues.
  • Obesity-associated PCT concentrations increased ROS and decreased NO in endothelial cells.
  • In vivo PCT administration impaired vasorelaxation and antagonized CGRP-induced NO release, dependent on CRLR/RAMP1.
  • Olcegepant and sitagliptin counteracted PCT-induced endothelial dysfunction.

Conclusions:

  • Adipose tissue-derived PCT exacerbates endothelial dysfunction in obesity by interfering with CGRP signaling.
  • Targeting hyperprocalcitonemia presents a potential strategy to maintain endothelial function and reduce obesity-related comorbidities.