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Published on: September 26, 2018
A simple method of plaque rupture induction in apolipoprotein E-deficient mice
Takeshi Sasaki1, Masafumi Kuzuya, Kae Nakamura
1Department of Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Arteriosclerosis, Thrombosis, and Vascular Biology
|April 1, 2006
Summary
Researchers developed a mouse model for atherosclerotic plaque rupture. This model uses apolipoprotein E-deficient mice and polyethylene cuffs to induce and study plaque rupture, aiding future research.
Area of Science:
- Cardiovascular Research
- Translational Medicine
- Animal Models
Background:
- Atherosclerosis is a leading cause of cardiovascular disease.
- Plaque rupture is a critical event leading to thrombotic complications.
- A reliable animal model is needed to study plaque rupture mechanisms.
Purpose of the Study:
- To develop a novel murine model for studying atherosclerotic plaque rupture.
- To establish a simple, fast, and efficient method for inducing plaque rupture in vivo.
- To provide a platform for evaluating therapeutic agents targeting plaque rupture.
Main Methods:
- Male apolipoprotein E (apoE)-deficient mice were used.
- Carotid artery ligation induced intimal hyperplasia.
- Polyethylene cuff placement near the ligation site triggered plaque rupture.
Main Results:
- Ligation led to lipid- and collagen-rich intimal hyperplasia with immune cell infiltration.
- Cuff placement induced intraplaque hemorrhage and plaque rupture.
- Rupture was associated with fibrin deposition, decreased collagen, and increased apoptosis.
Conclusions:
- A simple, fast, and efficient murine model of human plaque rupture was established.
- This model facilitates understanding of plaque rupture mechanisms.
- The model can be used to assess agents targeting plaque rupture.
