mProX™ Human CCR2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Knockdown of CCR2 in Pca cells induced Pca cell invasion
C4-2B and PC3 cells were stably-transfected with siRNA targeting of either CCR2 or a scrambled control. The clone with the strongest inhibition was presented. Representative micrographs and quantitative data for Pca invasion assay. MCP-1 (10 ng/ml) was added to the lower chambers. *P<0.001, significant difference from the controls.
Ref: Lu, Yi, et al. "Activation of MCP-1/CCR2 axis promotes prostate cancer growth in bone." Clinical & experimental metastasis 26 (2009): 161-169.
Pubmed: 19002595
DOI: 10.1007/s10585-008-9226-7
Research Highlights
Sasaki T, et al. "Progranulin deficiency exacerbates cardiac remodeling after myocardial ." FASEB bioAdvances, 2023.
Myocardial infarction (MI) is a fatal condition that leads to permanent death of heart muscle cells and subsequent changes in the cardiovascular system. Previous studies have shown that recombinant progranulin (PGRN) can protect against myocardial injury caused by lack of oxygen and subsequent restoration of blood flow. However, the role of PGRN after MI is still unclear. In this study, the effects of PGRN deficiency on cardiac changes after MI were investigated. Both wild-type and PGRN-knockout mice were used to analyze heart tissue, electrical activity, and protein levels. The levels of different types of immune cells in the heart were measured using flow cytometry. Furthermore, bone marrow-derived macrophages were collected and treated with different substances to assess gene expression and phagocytic ability. The results showed that PGRN levels gradually increased after MI, particularly in the border areas of the heart. Mice lacking PGRN had a higher mortality rate, more severe fibrosis of the heart, and increased occurrence of abnormal heart rhythms after MI. PGRN deficiency was also associated with higher levels of a specific type of macrophage and increased infiltration of immune cells in the damaged heart tissue. The PGRN-deficient macrophages were more reactive to certain substances and had altered expression of genes involved in immune response and tissue repair. This suggests that PGRN plays an important role in the proper initiation of heart repair and the polarization of macrophages after MI.
Pubmed:
37810172
DOI:
10.1096/fba.2023-00084
Jin L, et al. "CCR2 monocytes as therapeutic targets for acute disc herniation and radiculopathy ." Osteoarthritis and cartilage, 2023.
The study being described focuses on the role of monocytes and their derivatives in the development and progression of disc herniation, a common health issue that causes back pain and radiculopathy. Specifically, the researchers used a mouse model to investigate the effects of CCR2(+) monocytes on local inflammatory responses, pain levels, and disc degeneration. Results showed an increase of CCR2(+) monocytes at the sites of disc herniation, along with elevated levels of inflammatory cytokines. Inhibition of CCR2 signaling was found to reduce these effects and may serve as a potential therapeutic target for disc herniation induced pain.
Pubmed:
37802464
DOI:
10.1016/j.joca.2023.08.014
