Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Hypomethylation of MIF and CD74 in dataset GSE75434 . (A-C) Methylation data quality control. (D) Genomic distribution of methylation probes. (E, F) Significantly reduced methylation levels at MIF and CD74 loci in IAs versus control arteries. ** and * indicate p-values less than 0.01 and 0.05, respectively.

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Methylation, Control

Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Cell-cell communication analysis. (A) Global communication network showing interaction strength between major cell types. (B) Interaction weights for MIF ligand-receptor pairs. (C) Chord diagram highlighting MIF-CD74/CD44 signaling between VSMCs and M1-like macrophages. (D) Increased interaction strength and number between secretory VSMCs and M1-like macrophages in IAs. (E) Differential signaling pathway activity between secretory VSMCs and M1-like macrophages across conditions. (F) Heatmap showing communication probability for key pathways between secretory VSMCs and M1-like macrophages. (G) Expression patterns of key MIF axis components (Mif, Cd74, Cd44) across cell types.

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Activity Assay, Expressing

Journal: Frontiers in Immunology

Article Title: Macrophage migration inhibitory factor–CD74 axis drives vascular smooth muscle cell–induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation

doi: 10.3389/fimmu.2025.1682762

Figure Lengend Snippet: Secretory VSMCs drive macrophage M1 polarization via the MIF-CD74 axis. (A, B) qPCR analysis of iNOS and Arg1 expression in macrophages following Transwell co-culture. Secretory VSMCs increase iNOS and decrease Arg1; anti-MIF antibody or CD74 inhibitor (BMS-582949) attenuates this effect. (C) Flow cytometry quantification of CD86 + macrophages. Secretory VSMCs increase CD86 + proportion; inhibition of MIF or CD74 reduces it. (D, E) qPCR validation of MIF knockdown efficiency in VSMCs and its effect on macrophage iNOS/Arg1 expression in co-culture. MIF knockdown reverses secretory VSMC-induced polarization. (F) Flow cytometry shows MIF knockdown reduces CD86 + macrophage proportion induced by secretory VSMCs. (G, H) qPCR analysis of macrophages treated with secretory VSMC conditioned medium (CM). CM increases iNOS and decreases Arg1; CD74 inhibition reverses this. (I) Flow cytometry shows CD74 inhibition reduces CM-induced increase in CD86 + macrophages. Data are mean ± SEM; P < 0.01, P < 0.05 versus control; ##P < 0.01, #P < 0.05 versus secretory VSMC group (One-way ANOVA with Tukey’s post hoc test).

Article Snippet: Experimental groups were: (1) Control VSMCs + Macrophages; (2) Secretory VSMCs + Macrophages; (3) Secretory VSMCs + Macrophages + 10 μg/mL anti-human MIF monoclonal antibody (Abcam); (4) Secretory VSMCs + Macrophages + 5 μM CD74 inhibitor BMS-582949 (MedChemExpress).

Techniques: Expressing, Co-Culture Assay, Flow Cytometry, Inhibition, Biomarker Discovery, Knockdown, Control