CCR2 & Macrophage

CCR2, also known as CC chemokine receptor type 2, is a receptor protein found on the surface of immune cells including macrophages. Chemokine receptors like CCR2 play crucial roles in guiding immune cells to sites of inflammation or infection in the body.

Fig.1 CCR2+ macrophages in specific diseases.¹

CCR2 is particularly significant in the recruitment of monocytes, which are precursor cells to macrophages, to sites of inflammation. When certain chemokines bind to CCR2, it triggers a signaling cascade that attracts monocytes to the inflamed tissue. Once recruited, monocytes can then differentiate into macrophages, which contribute to the immune response by phagocytosing pathogens, producing inflammatory mediators, and facilitating tissue repair. The interaction between CCR2 and macrophages plays a crucial role in orchestrating the immune response to infection, inflammation, and tissue damage. Dysfunction in this interaction can contribute to various inflammatory diseases and conditions. Creative Biolabs offers tissue-specific macrophage-blocking services based on CCR2 knockout to help you accelerate your specific research on macrophages.

Our CCR2 Knockout-based Tissue-specific Macrophage Blocking Service

The interaction between CCR2 and macrophages plays a crucial role in orchestrating the immune response to infection, inflammation, and tissue damage. Dysfunction in this interaction can contribute to various inflammatory diseases and conditions. Creative Biolabs is committed to creating a comprehensive one-stop macrophage blockade service platform, we provide but are not limited to the following services. If you have any other special customization requirements, you can contact us directly.

• Specific animal model
• Flow cytometry
• Cardiac MRI
• Ambulatory ECG telemetry
• Bone marrow transplantation
• CCR2+ macrophage density analysis
• Real-time qPCR
• scRNA-seq
• Differential expression and gene set enrichment analyses

For more Tissue-specific Macrophage Blocking Services, please click here!

Published Data

• Background

This study validates that CCR2-recruited macrophages upregulate SPP1 expression in both human and mouse atrium, thereby exacerbating inflammation and fibrosis. Through these processes, macrophages contribute to the electrophysiological basis of atrial fibrillation, resulting in atrial fibrillation.

• Results Display

Single-cell atlas of human atrial disease.
Fig.2 Single-cell atlas of human atrial disease.2	The results showed that the ratio of MP/DC cells (mononuclear phagocytes and dendritic cells) in six types of non-myocardial cells in cardiac tissue was significantly increased. Correspondingly, the expression of inflammatory and pro-fibrotic genes, such as CCR2, IL10, SPP1, etc., was also significantly increased. In addition, in MP/DC cells, a macrophage with high levels of SPP1 expression was also significantly expanded.
Single-cell atlas of mouse model
Fig.3 Single-cell atlas of mouse model.2	Then, the animal model was validated. The HOMER (hypertension, obesity, and mitral regurgitation) model mouse was established, which can induce atrial fibrillation with left atrial enlargement. Through single-cell sequencing of the heart of the HOMER mouse model, they confirmed the recruitment of SPP1-expressing macrophages in the heart during atrial fibrillation.
Effect of CCR2-dependent monocyte recruitment
Fig.4 Effect of CCR2-dependent monocyte recruitment.2	Because atrial macrophages were enriched in HOMER mice, the chemokine receptor CCR2 was recruited to express macrophages. They hypothesized that atrial fibrillation was caused by the recruitment of macrophages in the atria due to the expression of CCR2. They knocked out CCR2 in mice and experimentally verified that inhibition of macrophage recruitment reduced atrial fibrillation.
Macrophage-derived SPP1 promotes atrial disease
Fig.5 Macrophage-derived SPP1 promotes atrial disease.2	The reason for recruiting macrophages was CCR2, and the macrophages that affect atrial fibrillation are highly expressing SPP1, so they hypothesized that there was a causal link between SPP1 and atrial fibrillation. HOMER model mice with SPP1 missing in bone marrow cells were relieved of symptoms of atrial fibrillation. The results showed that CD68 macrophages in heart tissue were also significantly reduced in mice lacking SPP1. The absence of SPP1 does not cause macrophage death. That is, SPP1 enhances atrial inflammation by increasing macrophage proliferation.

As a leading provider in the field of macrophage R&D, Creative Biolabs provides you with one-stop macrophage services, including cell culture, characterization, reprogramming, engineering, etc. If you're interested, you can click on keywords for more information.