Journal: Advanced Science

Article Title: Alternating Shear Force of Respiration Regulates Cell Interactions of Fibroblasts and Macrophages to Promote Soft Tissue Integration of Chest Wall Polyetheretherketone Implants

doi: 10.1002/advs.77118

Figure Lengend Snippet: Mechanical force modulates macrophage M2 polarization on PEEK surfaces. (A) The expression levels of mechanical perception (PIEZO1, YAP1) and polarization‐related proteins (iNOS, CD206, STAT6/p‐STAT6, NF‐κB/p‐NF‐κB) in dynamically cultured RAW264.7, determined by Western blot. (B) Gene expression in RAW264.7 were cultured under dynamic and static conditions for 12 h. (C) SEM images of RAW264.7 under static and dynamic culture conditions (scale bar: 10 µm). (D) Confocal fluorescence images of CD206, PIEZO1, iNOS, IL10, YAP1 and ITGB1 in macrophages under dynamic and static conditions (scale bar: 100 µm). The average fluorescence intensity of (E) CD206, IL‐10, (F) PIEZO1, YAP1, and (G) iNOS, ITGB1 were statistically analyzed. Shown are mean values ± SD (n = 3 independent experiments, each with 3 technical replicates), * P < 0.05, ** P < 0.01, and *** P < 0.001, ns, no significant difference. 2‐way ANOVA was used in (B) and (E–G).

Article Snippet: To induce M2 phenotype, M0 macrophages were stimulated with 10 ng/mL IL‐10 (HY‐P70517, MedChemExpress LLC., USA) and 20 ng/mL IL‐4 (HY‐ P70653 , MedChemExpress LLC., USA)

Techniques: Expressing, Cell Culture, Western Blot, Gene Expression, Fluorescence

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: For mouse experiments, mouse IL-10 was measured using the Mouse IL-10 ELISA Kit (R&D Systems, Cat# M1000B), and mouse TGF-β1 was measured using the Mouse TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS608-4), following the manufacturers’ instructions.

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: Human IL-10 was quantified using IL-10 DuoSet ELISA (R&D Systems, Cat# DY217B), and human TGF-β1 was measured using the Human TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS249-4).

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Journal: Bioactive Materials

Article Title: Glucose/ROS-responsive and redox-gated adaptive hydrogel dressing for accelerating diabetic wound repair via synergistic cGAS/STING pathway inhibition and oxidative stress alleviation

doi: 10.1016/j.bioactmat.2026.03.025

Figure Lengend Snippet: Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and IL-10, and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).

Article Snippet: IL-6 and IL-10-specific antibodies were purchased from Bosterbio (Wuhan, China).

Techniques: Immunofluorescence, Staining, Fluorescence

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: Human IL-10 was quantified using IL-10 DuoSet ELISA (R&D Systems, Cat# DY217B), and human TGF-β1 was measured using the Human TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS249-4).

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Journal: Frontiers in Immunology

Article Title: Single-cell and spatial profiling reveal an IL-10–associated iCAF–M2 macrophage communication axis in high-grade serous ovarian cancer ascites

doi: 10.3389/fimmu.2026.1790912

Figure Lengend Snippet: IL10 blockade with MK-1966 suppresses tumor growth and decreases IL10 pathway activity in humanized PDX models. (A) Schematic of humanized ovarian cancer PDX model generation and MK-1966 treatment timeline. (B) Representative tumor images demonstrating visibly smaller tumors in MK-1966–treated mice. (C) Tumor growth curves showing significantly reduced tumor volume following MK-1966 treatment (n = 5, p < 0.001). (D) Final tumor weight demonstrating significantly lower tumor mass in treated mice (n = 5, p < 0.001). (E) Representative IHC staining showing decreased CD206, Ki67, IL-10, and IL-10RA expression in MK-1966 tumors versus controls. (F) Quantitative IHC scoring confirming significant reductions in CD206 and Ki67 ( p < 0.01) and IL-10 and IL-10RA ( p < 0.05) following treatment. N = 3 (G) Representative multiplex immunofluorescence staining of DAPI (blue), EpCAM (green), and Ki67 (red) demonstrating co-localization of Ki67-positive proliferating cells within EpCAM-positive tumor cells. MK-1966 treatment markedly reduced EpCAM + /Ki67 + double-positive tumor cells compared with controls. (H) Quantitative analysis of EpCAM + /Ki67 + relative fluorescence intensity demonstrating significantly decreased tumor-cell proliferative activity following MK-1966 treatment (** p< 0.01). * represent p-value < 0.05; *** represent p-value < 0.001.

Article Snippet: Once tumors reached ~100 mm3, animals were randomized into: Control group (vehicle) and MK-1966 treatment group (anti-IL-10 monoclonal antibody; MCE, HY-P991257).

Techniques: Activity Assay, Immunohistochemistry, Expressing, Multiplex Assay, Immunofluorescence, Staining, Fluorescence