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Related Experiment Video

Updated: Sep 27, 2025

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
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Angiotensin II Induces Aortic Rupture and Dissection in Osteoprotegerin-Deficient Mice.

Toshihiro Tsuruda1, Atsushi Yamashita2, Misa Otsu1

  • 1Division of Internal Medicine, Cardiovascular Medicine and Nephrology Faculty of Medicine University of Miyazaki Japan.

Journal of the American Heart Association
|April 12, 2022
PubMed
Summary

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Osteoprotegerin protects against aortic rupture and dissection in angiotensin II-induced hypertension. Its absence worsens aortic integrity by increasing soluble receptor activator of nuclear factor-kappa B ligand activity and periostin expression.

Area of Science:

  • Cardiovascular Biology
  • Vascular Medicine
  • Hypertension Research

Background:

  • Osteoprotegerin (OPG) is a soluble decoy receptor for receptor activator of nuclear factor-kappa B ligand (RANKL).
  • The precise role of OPG in vascular structure, particularly in hypertension-induced aortic complications, remains unclear.
  • Understanding OPG's mechanism is crucial for developing targeted therapies for aortic diseases.

Purpose of the Study:

  • To investigate the effect of osteoprotegerin on aortic structural integrity in a mouse model of angiotensin II-induced hypertension.
  • To elucidate the biological mechanism by which OPG influences aortic complications.

Main Methods:

  • Utilized osteoprotegerin gene-knockout mice and wild-type littermates subjected to angiotensin II infusion.
Keywords:
aortic dissectionelastinextracellular matrixproteoglycan

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  • Assessed mortality, aortic rupture, aortic dissection, medial and adventitial thickness, elastin breaks, periostin expression, and soluble RANKL concentrations.
  • Administered PEGylated human recombinant osteoprotegerin to knockout mice to evaluate therapeutic potential.

    • Main Results:

    • Osteoprotegerin gene-knockout mice exhibited significantly higher mortality, aortic rupture, and dissection rates compared to wild-type mice under angiotensin II infusion.
    • Absence of OPG correlated with reduced aortic wall thickness, increased elastin fragmentation, elevated periostin expression, and higher soluble RANKL levels.
    • Recombinant OPG administration markedly reduced mortality, aortic dissection, elastin breaks, periostin expression, and soluble RANKL levels in knockout mice.

    Conclusions:

    • Osteoprotegerin plays a critical protective role in maintaining aortic structural integrity during angiotensin II-induced hypertension.
    • OPG mitigates aortic rupture and dissection by inhibiting RANKL activity and periostin expression.
    • These findings highlight OPG as a potential therapeutic target for preventing aortic complications in hypertensive individuals.