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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Dectin-1 deficiency does not affect atherosclerosis development in mice.

Katka Szilagyi¹, Marion J J Gijbels², Saskia van der Velden³

¹Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Atherosclerosis

|February 16, 2015

Summary

This summary is machine-generated.

Dectin-1 deficiency did not alter atherosclerotic plaque development or macrophage function in mice. This suggests dectin-1 (dectin-1) is not essential for atherosclerosis progression.

Keywords:

Atherosclerosis Dectin-1 Macrophages Respiratory burst

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Last Updated: Apr 17, 2026

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Published on: September 26, 2018

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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

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Published on: December 7, 2013

Area of Science:

Immunology
Cardiovascular Research

Background:

Emerging evidence implicates dectin-1 in atherosclerosis via reactive oxygen species (ROS) modulation.
Dectin-1 is a receptor expressed on myeloid cells, including macrophages.

Purpose of the Study:

To investigate the impact of dectin-1 deficiency on the development of atherosclerotic plaques.
To determine if dectin-1 plays a role in regulating ROS production within atherosclerotic lesions.

Main Methods:

Immunohistochemistry was used to detect dectin-1 expression on macrophages in mouse atherosclerotic lesions.
Low-density lipoprotein receptor-deficient (LDLR(-/-)) mice were lethally irradiated and reconstituted with bone marrow from wild-type or dectin-1-deficient (dectin-1(-/-)) mice.
Mice were fed a high-fat diet for 9 weeks to induce atherosclerosis, followed by lesion analysis.

Main Results:

No significant differences in atherosclerotic plaque size or severity were observed between dectin-1 deficient and wild-type groups.
Macrophage and granulocyte composition within plaques remained similar across both experimental groups.
The capacity of macrophages to produce reactive oxygen species (ROS) was not affected by dectin-1 deficiency.

Conclusions:

Dectin-1 is dispensable for the development of atherosclerotic lesions in this mouse model.
The study findings indicate that dectin-1 does not play a critical role in regulating atherosclerosis progression or associated macrophage inflammatory responses.