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Published on: April 3, 2017
The orphan receptor GPRC5B promotes macrophage infiltration and an inflammatory plaque phenotype in atherosclerosis
Greta Verena Freundt1, Friedrich Alexander von Samson-Himmelstjerna1, Jan-Thorge Nitz1
1Department of Cardiology and Angiology, University Hospital Schleswig-Holstein, Campus Kiel, Christian-Albrechts-Universität zu Kiel, Arnold-Heller-Str. 3, D-24105 Kiel, Germany.
Background And Aims:
Atherosclerosis is driven by chronic inflammation of the vascular wall, in which macrophages play a central role. The orphan G protein-coupled receptor GPRC5B is expressed in vascular cells and macrophages and is upregulated during monocyte-to-macrophage differentiation. It has been shown to activate NFκB-dependent inflammatory pathways in adipose tissue and glomeruli. Here, we investigated the impact of GPRC5B on macrophage infiltration and the progression of atherosclerotic plaque development in vivo.
Methods:
Bone marrow from heterozygous GPRC5B-transgenic C57BL/6 mice and wild-type controls was transplanted into lethally irradiated LDL receptor-deficient mice. Animals were fed a Western-type diet for 16 weeks, after which atherosclerotic lesions in the aortic sinus were analyzed.
Results:
Mice receiving GPRC5B-transgenic bone marrow showed no significant differences in serum lipids or cardiac mass indices. However, they exhibited significantly increased macrophage infiltration within atherosclerotic plaques and a non-significant trend toward larger and more complex lesions.
Conclusions:
GPRC5B overexpression in bone marrow-derived monocyte/macrophage lineage cells promotes a more inflammatory plaque phenotype, characterized by enhanced macrophage infiltration. These findings highlight GPRC5B as a potential modulator of plaque progression and suggest it may represent a novel therapeutic target in vascular inflammation and atherosclerosis.
Insights
Overexpression of G protein-coupled receptor GPRC5B in macrophages promotes plaque inflammation and macrophage infiltration in atherosclerosis. This suggests GPRC5B may be a therapeutic target for vascular inflammation.
Area of Science:
- Cardiovascular Research
- Immunology
- Molecular Biology
Background:
- Atherosclerosis involves chronic vascular wall inflammation with macrophages playing a key role.
- G protein-coupled receptor GPRC5B (GPRC5B) is present in vascular cells and macrophages, increasing during differentiation.
- GPRC5B activates inflammatory pathways in adipose tissue and glomeruli.
Purpose of the Study:
- To investigate the role of GPRC5B in macrophage infiltration.
- To determine the impact of GPRC5B on atherosclerotic plaque progression in vivo.
Main Methods:
- Bone marrow from GPRC5B-transgenic and wild-type mice was transplanted into LDL receptor-deficient mice.
- Mice were fed a Western-type diet for 16 weeks.
- Atherosclerotic lesions in the aortic sinus were analyzed.
Main Results:
- No significant differences in serum lipids or cardiac mass were observed.
- GPRC5B-transgenic mice showed significantly increased macrophage infiltration in plaques.
- A trend towards larger and more complex lesions was noted.
Conclusions:
- GPRC5B overexpression enhances macrophage infiltration, promoting a more inflammatory plaque phenotype.
- GPRC5B is a potential modulator of atherosclerotic plaque progression.
- GPRC5B may serve as a novel therapeutic target for vascular inflammation.
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