Mouse CCL7/MCP-3/MARC Antibody

Chemotaxis Induced by CCL7/MARC and Neutralization by Mouse CCL7/MARC Antibody. Recombinant Mouse CCL7/ MARC (Catalog # 456-MC) chemoattracts the BaF3 mouse pro-B cell line transfected with human CCR2A in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (Catalog # AR002). Chemotaxis elicited by Recombinant Mouse CCL7/ MARC (2 µg/mL) is neutralized (green line) by increasing concentrations of Mouse CCL7/MARC Antigen Affinity-purified Polyclonal Antibody (Catalog # AF-456-NA). The ND₅₀ is typically 7.5-45 µg/mL.

Detection of CCL7/MCP-3/MARC by Western Blot CCL7‐activated JAK2/STAT1 signal in macrophages. (A) Protein abundance of JAK2 and STAT1 in abdominal aortas of saline (n = 4) and Ang II‐infused (n = 4) mice. (B) Protein abundance of JAK2, p‐JAK2, STAT1, p‐STAT1 and p‐JAK2/JAK2, p‐STAT1/STAT1 ratio in BMDMs incubated with rmCCL7 (100 ng/ml). (C) Protein abundance of STAT1, p‐STAT1 and p‐STAT1/STAT1 ratio in BMDM incubated with rmCCL7(100 ng/ml) and pre‐treated 1 hour with JAK2 inhibitor Fedratinib (1 μM). Values were represented as mean ± SEM; Student's t test was used for data analysis in (A, B). One Way ANOVA was used for data analysis in(C). *P < .05; **P < .01; ***P < .001, respectively Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34189838), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CCL7/MCP-3/MARC by Western Blot CCL7‐CCR1 interaction regulated macrophage phenotype through JAK2 /STAT1 pathway. (A) Protein abundance of JAK2, p‐JAK2, STAT1, p‐STAT1 and p‐JAK2/JAK2, p‐STAT1/STAT1 ratio in BMDMs incubated with rmCCL7 (100 ng/ml) and pre‐treated 1 hour with CCR1 antagonist‐BX471(1 μM and 10 μM). (B) M1 markers (iNOS, IL‐6, IL‐12A, IL‐12B, TNF‐ alpha ) mRNA level in BMDMs incubated with rmCCL7 alone or in combination with JAK2 inhibitor‐Fedratinib (1 μM) and STAT1 inhibitor‐Fludarabine (1 μM). (C) Pathological mechanism diagram of CCL7 in Ang II‐induced AAA. Values were represented as mean ± SEM; One Way ANOVA was used for data analysis in (A‐B) *P < .05; **P < .01; ***P < .001, respectively Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34189838), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CCL7/MCP-3/MARC by Western Blot CCL7 expression and macrophages infiltration increased in Ang II‐infused abdominal aortas. (A) Representative abdominal aorta images with ultrasound examination, the maximum abdominal aorta diameter (luminal diameter) and the maximum abdominal aorta area (luminal area). A grid on the scale represented 0.5 mm. (B) qRT‐PCR for CCL7 mRNA expression in saline (n = 6) and Ang II (n = 7) infused mice. (C) Protein levels of CCL7 in saline (n = 6) and Ang II (n = 7) infused abdominal aortas. (D) Plasma concentrations of CCL7 in saline (n = 6) and Ang II (n = 9) infused mice. (E) Representative images of macrophage infiltration in aneurysmal lesions as revealed by CD68 immunostaining. Black arrows indicated CD68‐positive location, scale bars represented 200 μm (left) and 50 μm (right images). Values were represented as mean ± SEM; Student's t test was used for data analysis in (A‐E). *P < .05; **P < .01; ***P < .001, respectively Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34189838), licensed under a CC-BY license. Not internally tested by R&D Systems.