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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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Adipose tissue macrophages do not affect atherosclerosis development in mice.
Mitchell Bijnen1, José van de Gaar1, Maria Vroomen1
1Dept. of Internal Medicine, MUMC, Maastricht, the Netherlands; CARIM, MUMC, Maastricht, the Netherlands.
Atherosclerosis
|January 18, 2019
Summary
Adipose tissue inflammation in obesity may drive atherosclerosis. However, adipose tissue macrophages (ATMs) from obese visceral adipose tissue (vAT) do not directly impact atherosclerotic plaque development or characteristics.
Area of Science:
- Immunology
- Cardiovascular Biology
- Metabolic Disease Research
Background:
- Obesity is linked to increased atherosclerosis risk, potentially mediated by adipose tissue (AT) inflammation.
- Adipose tissue macrophages (ATMs) in obese AT recruit immune cells from bone marrow.
- The direct role of ATMs in atherosclerotic plaque development requires investigation.
Purpose of the Study:
- To determine if ATMs directly contribute to atherosclerotic plaque development.
- To investigate the influence of ATMs from obese visceral AT (vAT) on atherosclerosis.
Main Methods:
- Lean LDL receptor-deficient (ldlr-/-) mice received visceral AT (vAT) transplants from lean, obese, or ATM-depleted obese donors.
- Mice were fed a high-cholesterol diet (HCD) to induce atherosclerosis post-transplantation.
- Atherosclerotic plaque development was assessed 8 weeks after vAT transplantation.
Main Results:
- Obese vAT transplantation altered circulating triglycerides, B-cells, and Ly6c- monocytes, but not cholesterol or other immune cells.
- Depleting ATMs from obese vAT prior to transplantation reversed these alterations, except for an increase in eosinophils.
- Neither obese vAT transplantation nor ATM depletion significantly affected atherosclerotic plaque size, phenotype, or stability.
Conclusions:
- Adipose tissue macrophages (ATMs) originating from obese visceral adipose tissue (vAT) do not directly influence the development or phenotype of atherosclerotic plaques.
- The inflammatory mediators produced by ATMs in obese AT may not be the primary drivers of atherosclerosis progression in this model.
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