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Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model

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Published on: August 25, 2020

Delayed arteriogenesis in hypercholesterolemic mice.

Daniela Tirziu¹, Karen L Moodie, Zhen W Zhuang

¹Angiogenesis Research Center, Department of Medicine, Dartmouth Medical School, Lebanon, NH, USA.

|October 19, 2005

Summary

This summary is machine-generated.

Hypercholesterolemia delays arterial growth (arteriogenesis) by reducing early immune cell arrival and impairing blood vessel repair. This hinders recovery after injury, even with growth factor treatment.

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Area of Science:

Cardiovascular Biology
Vascular Biology
Regenerative Medicine

Background:

Hypercholesterolemia is known to impede angiogenesis (new blood vessel formation).
Its impact on arteriogenesis (arterial remodeling and growth) remains less understood.

Purpose of the Study:

To investigate the effects of hypercholesterolemia on arteriogenesis.
To evaluate arterial growth in hypercholesterolemic mice.

Main Methods:

Hypercholesterolemic low-density lipoprotein receptor(-/-)/ApoB-48(-/-) (HCE) mice and control mice underwent femoral artery ligation.
Vascular growth and limb perfusion were assessed using micro-computed tomography, MRI, and laser Doppler imaging.
Gene expression analysis was performed post-treatment with Ad-PR39.

Main Results:

Untreated HCE mice showed significantly delayed restoration of limb perfusion compared to controls.
Growth factor therapy (Ad-PR39) demonstrated a delayed and impaired arteriogenesis response in HCE mice.
Delayed arteriogenesis in HCE mice correlated with reduced early monocyte/macrophage infiltration and altered gene expression.

Conclusions:

Hypercholesterolemia significantly delays native arteriogenesis.
This delay is attributed to reduced early monocyte/macrophage influx.
Hypercholesterolemia impairs arterial growth response to growth factor therapy.