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Apelin prevents aortic aneurysm formation by inhibiting macrophage inflammation

Nicholas J Leeper1, Maureen M Tedesco, Yoko Kojima

  • 1Division of Cardiovascular Medicine, Department of Medicine, Stanford Univ., 300 Pasteur Dr., Stanford, California 94305, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|March 24, 2009
PubMed

Insights

Apelin, a potent inodilator, significantly reduces abdominal aortic aneurysm (AAA) formation by decreasing vascular inflammation and macrophage infiltration. This study highlights apelin

Area of Science:

  • Vascular Biology
  • Cardiovascular Research
  • Inflammation and Immunology

Background:

  • Apelin is an inodilator with known antiatherogenic effects.
  • Vascular wall inflammation is a key factor in abdominal aortic aneurysm (AAA) development.
  • The potential of apelin to mitigate AAA formation by reducing inflammation requires investigation.

Purpose of the Study:

  • To investigate the hypothesis that apelin attenuates abdominal aortic aneurysm (AAA) formation.
  • To determine if apelin limits disease-related vascular wall inflammation in AAA.
  • To assess the impact of apelin on inflammatory cell infiltration and cytokine expression in AAA.

Main Methods:

  • Apelin or saline was administered to C57BL/6 mice via osmotic pumps.
  • Infrarenal abdominal aortic aneurysms (AAAs) were induced using pancreatic elastase.
  • Aortic dimensions and macrophage infiltration were assessed using ultrasonography and histology.
  • Gene expression of inflammatory markers was analyzed via PCR in aortic tissues and cultured cells.

Main Results:

  • Apelin treatment significantly reduced AAA formation, decreasing maximal cross-sectional area by 47% and macrophage infiltrate by 57%.
  • Apelin infusion led to reduced expression of macrophage colony-stimulating factor, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha).
  • Apelin stimulation of cultured macrophages decreased MCP-1 and TNF-alpha mRNA levels but did not affect adhesion molecule expression or cytokine production in other vascular cells.

Conclusions:

  • Apelin significantly reduces aneurysm formation in a mouse model of AAA.
  • The mechanism involves a decreased macrophage burden, likely due to apelin-mediated reduction in pro-inflammatory cytokine and chemokine activation.
  • Apelin demonstrates therapeutic potential for mitigating AAA development by targeting vascular inflammation.

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