Source Paper
Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata
Filip K. Swirski, Peter Libby, Elena Aikawa, Pilar Alcaide, F. William Luscinskas et al.
Journal of Clinical Investigation • 2007
High-Fat Diet Atherosclerosis Model
Objective: To investigate the role of Ly-6C hi monocytes in hypercholesterolemia-associated monocytosis and atherosclerosis development in apoE-deficient mice consuming a high-fat diet
This is a High-Fat Diet Atherosclerosis Model protocol using mouse as the model organism. The procedure involves 3 procedural steps, 1 materials. Extracted from a 2007 paper published in Journal of Clinical Investigation.
Model and subjects
mouse • apoE-deficient • unknown • Not specified • Not specified
Study window
Estimated timing pending
Core workflow
High-fat diet administration • Monocyte monitoring and characterization • Statin treatment (optional endpoint)
Primary readouts
- Ly-6C hi monocyte numbers in blood (doubling rate per month)
- Ly-6C lo monocyte numbers (remained unaffected)
- Monocyte adhesion to activated endothelium
- Monocyte infiltration into atherosclerotic lesions
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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High-fat diet administration
apoE-deficient mice were fed a high-fat diet to induce hypercholesterolemia and atherosclerosis
Note: Mice were monitored for development of hypercholesterolemia-associated monocytosis (HAM)
View evidence from paper
“hypercholesterolemic apoE–deficient mice consuming a high-fat diet, with the number of Ly-6C hi cells doubling in the blood every month”
Monocyte monitoring and characterization
Circulating monocytes were monitored for Ly-6C hi and Ly-6C lo subsets; Ly-6C hi monocytes were tracked for adhesion to activated endothelium and infiltration into lesions
Note: Ly-6C hi monocytes were observed to adhere to activated endothelium, infiltrate lesions, and become lesional macrophages
View evidence from paper
“Ly-6C hi monocytes adhered to activated endothelium, infiltrated lesions, and became lesional macrophages”
Statin treatment (optional endpoint)
Statin-induced cholesterol reduction was used to assess whether HAM subsided upon cholesterol reduction
Note: This was used as a control condition to demonstrate reversibility of the monocytosis
View evidence from paper
“subsided upon statin-induced cholesterol reduction”