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vascular endothelial growth factor  (R&D Systems)


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    R&D Systems vascular endothelial growth factor
    Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and <t>VEGF</t> expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    Vascular Endothelial Growth Factor, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 441 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+vegf/Human+VEGF+DuoSet+ELISA/pmc12926579-106-14-25
    Average 96 stars, based on 441 article reviews
    vascular endothelial growth factor - by Bioz Stars, 2026-10
    96/100 stars

    Images

    1) Product Images from "Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing"

    Article Title: Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.02.004

    Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    Figure Legend Snippet: Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Techniques Used: Activity Assay, Gene Expression, Activation Assay, Inhibition, Marker, Expressing

    Pro-inflammatory (M1) macrophages are driven towards an anti-inflammatory (M2) phenotype on CG-155-i scaffolds. A-B) Assessment of cell viability through metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Scaffold-mediated inhibition of miRNA-155 in pro-inflammatory macrophages maintains SHIP1 and SOCS1 upregulation despite the enhanced inflammatory environment. F-H) NOS2 expression shows a trending decrease while CD80 and CD86 levels are downregulated on the CG-155-i scaffolds. I-J) Scaffold-mediated miRNA-155 inhibition does not significantly alter ARG1 expression whereas CD206 is still upregulated, highlighted an M2 macrophage polarisation despite the inflammatory cues. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    Figure Legend Snippet: Pro-inflammatory (M1) macrophages are driven towards an anti-inflammatory (M2) phenotype on CG-155-i scaffolds. A-B) Assessment of cell viability through metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Scaffold-mediated inhibition of miRNA-155 in pro-inflammatory macrophages maintains SHIP1 and SOCS1 upregulation despite the enhanced inflammatory environment. F-H) NOS2 expression shows a trending decrease while CD80 and CD86 levels are downregulated on the CG-155-i scaffolds. I-J) Scaffold-mediated miRNA-155 inhibition does not significantly alter ARG1 expression whereas CD206 is still upregulated, highlighted an M2 macrophage polarisation despite the inflammatory cues. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Techniques Used: Activity Assay, Inhibition, Expressing

    Secretome from macrophages cultured on CG-155-i scaffolds induces anti-inflammatory responses on endothelial cells. A) Cytokine profile analysis revealed an increased release of pro-angiogenic and anti-inflammatory growth factors from macrophages on CG-155-i scaffolds. B-E) Endothelial cells exposed to M0 macrophage secretome show a reduced expression of pro-inflammatory ICAM in the CG-155-i group. F-I) M1 macrophage secretome on endothelial cells elicits clear morphological changes and decreased ICAM intensity in the CG-155-i group. Scale bars = 100 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01.
    Figure Legend Snippet: Secretome from macrophages cultured on CG-155-i scaffolds induces anti-inflammatory responses on endothelial cells. A) Cytokine profile analysis revealed an increased release of pro-angiogenic and anti-inflammatory growth factors from macrophages on CG-155-i scaffolds. B-E) Endothelial cells exposed to M0 macrophage secretome show a reduced expression of pro-inflammatory ICAM in the CG-155-i group. F-I) M1 macrophage secretome on endothelial cells elicits clear morphological changes and decreased ICAM intensity in the CG-155-i group. Scale bars = 100 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01.

    Techniques Used: Cell Culture, Expressing

    Secretome from macrophages on CG-155-i scaffolds enhances endothelial cell migration and organisation into vascular-like structures under chronic-like conditions. A) Endothelial cells exposed to M1 macrophage secretome show reduced migration rates compared to M0 conditions. B-C) Analysis of migration profiles under M0 conditions did not reveal any clear differences in behaviour between treatment groups. D-E) Endothelial cell migration rate exposed to secretome from M1 macrophages on CG-155-i scaffolds result in faster cell migration compared to the negative and miRNA-free groups after 24 h. E) Endothelial cells show higher vascular-like organisation when exposed to M0 macrophage secretome. F-H) Secretome from CG-155-i scaffolds enables improved vascular-like complexity in both M0 and M1 conditions. Scale bars = 500 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p > 0.001, and ∗∗∗∗p < 0.0001.
    Figure Legend Snippet: Secretome from macrophages on CG-155-i scaffolds enhances endothelial cell migration and organisation into vascular-like structures under chronic-like conditions. A) Endothelial cells exposed to M1 macrophage secretome show reduced migration rates compared to M0 conditions. B-C) Analysis of migration profiles under M0 conditions did not reveal any clear differences in behaviour between treatment groups. D-E) Endothelial cell migration rate exposed to secretome from M1 macrophages on CG-155-i scaffolds result in faster cell migration compared to the negative and miRNA-free groups after 24 h. E) Endothelial cells show higher vascular-like organisation when exposed to M0 macrophage secretome. F-H) Secretome from CG-155-i scaffolds enables improved vascular-like complexity in both M0 and M1 conditions. Scale bars = 500 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p > 0.001, and ∗∗∗∗p < 0.0001.

    Techniques Used: Migration

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    Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and <t>VEGF</t> expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    Human Vegf Elisa Kit, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Functional characterization of AdMSC spheroids and their integration with GC. (a) Bright-field images and size distribution of spheroids generated in agarose molds targeting a diameter of 300 μm. (b) Representative confocal images of hypoxic core staining in spheroids, showing nuclei (blue) and hypoxic regions (green). (c, d) ELISA quantification of cumulative VEGF and HGF secretion from 2D-cultured AdMSCs and spheroids after 3 days culture. (e) Bright-field and confocal fluorescence images of spheroids alone, spheroids exposed to blue light (B.L), spheroids encapsulating 5% (w/v) gelatin hydrogel, or spheroids encapsulating 4–7% (w/v) GCs and photo-crosslinked under 450 nm blue light. Samples were stained with phalloidin (green, F-actin) and DAPI (blue, nuclei); dotted boxes indicate magnified regions. (f) Quantification of normalized cell proliferation within the GC in each condition over 1, 3, and 5 days incubation (n = 3). (g) Cumulative VEGF secretion from encapsulated spheroids measured at 1, 3, and 5 days (n = 5). (h) Spheroid diameter measurements over the incubation period, indicating the degree of spheroid spreading within each matrix (n = 10). (i) Representative HUVEC tube formation images after treatment with conditioned media from VEGF-free control (-VEGF), VEGF-supplemented media (+VEGF), spheroids alone, spheroid encapsulating 5% (w/v) GC, or spheroid encapsulating 7% (w/v) GC groups. (j–m) Quantitative tube formation parameters, including total tube length, number of meshes, number of junctions, and total mesh area, respectively (n = 4). (n) Representative Annexin V-FITC/propidium iodide flow cytometry plots of H 2 O 2 -treated SG cells in the absence or presence of spheroid encapsulating 5% (w/v) GC or spheroid encapsulating 7% (w/v) GCs. (o) Quantification of live, early apoptotic, and late apoptotic cell populations under each condition (n = 3). (p) Relative M2/M1 polarization of macrophages after LPS stimulation and treatment with conditioned media with spheroids and spheroids encapsulating GCs as determined by ELISA (n = 3). Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. ns P > 0.05, ∗ P ≤ 0.05, ∗∗ P ≤ 0.01, and ∗∗∗ P ≤ 0.001.

    Journal: Bioactive Materials

    Article Title: AdMSC spheroids encapsulating antioxidant hybrid protein carrier for irradiation-damaged salivary gland repair

    doi: 10.1016/j.bioactmat.2026.03.049

    Figure Lengend Snippet: Functional characterization of AdMSC spheroids and their integration with GC. (a) Bright-field images and size distribution of spheroids generated in agarose molds targeting a diameter of 300 μm. (b) Representative confocal images of hypoxic core staining in spheroids, showing nuclei (blue) and hypoxic regions (green). (c, d) ELISA quantification of cumulative VEGF and HGF secretion from 2D-cultured AdMSCs and spheroids after 3 days culture. (e) Bright-field and confocal fluorescence images of spheroids alone, spheroids exposed to blue light (B.L), spheroids encapsulating 5% (w/v) gelatin hydrogel, or spheroids encapsulating 4–7% (w/v) GCs and photo-crosslinked under 450 nm blue light. Samples were stained with phalloidin (green, F-actin) and DAPI (blue, nuclei); dotted boxes indicate magnified regions. (f) Quantification of normalized cell proliferation within the GC in each condition over 1, 3, and 5 days incubation (n = 3). (g) Cumulative VEGF secretion from encapsulated spheroids measured at 1, 3, and 5 days (n = 5). (h) Spheroid diameter measurements over the incubation period, indicating the degree of spheroid spreading within each matrix (n = 10). (i) Representative HUVEC tube formation images after treatment with conditioned media from VEGF-free control (-VEGF), VEGF-supplemented media (+VEGF), spheroids alone, spheroid encapsulating 5% (w/v) GC, or spheroid encapsulating 7% (w/v) GC groups. (j–m) Quantitative tube formation parameters, including total tube length, number of meshes, number of junctions, and total mesh area, respectively (n = 4). (n) Representative Annexin V-FITC/propidium iodide flow cytometry plots of H 2 O 2 -treated SG cells in the absence or presence of spheroid encapsulating 5% (w/v) GC or spheroid encapsulating 7% (w/v) GCs. (o) Quantification of live, early apoptotic, and late apoptotic cell populations under each condition (n = 3). (p) Relative M2/M1 polarization of macrophages after LPS stimulation and treatment with conditioned media with spheroids and spheroids encapsulating GCs as determined by ELISA (n = 3). Data are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. ns P > 0.05, ∗ P ≤ 0.05, ∗∗ P ≤ 0.01, and ∗∗∗ P ≤ 0.001.

    Article Snippet: VEGF and HGF levels were quantified using human VEGF (ABclonal, RK00023) and human HGF ELISA kits according to the manufacturers’ protocols, and absorbance was read at 450 nm with 540 nm reference using a microplate reader (VersaMax; Molecular Devices, USA).

    Techniques: Functional Assay, Generated, Staining, Enzyme-linked Immunosorbent Assay, Cell Culture, Fluorescence, Incubation, Control, Flow Cytometry

    Angiogenic effect of spheroids encapsulating GC for IR-damaged salivary glands. (a) Immunofluorescence staining for CD31 (green), an endothelial cell marker, in SG tissue sections to evaluate neovascularization. (b, c) Quantification of CD31-positive areas at 1 and 6 weeks post-treatment. (d) Immunofluorescence staining for VEGF-A (red), an angiogenesis marker, in SG tissue sections. (e, f) Quantification of VEGF-A-positive areas at 1 and 6 weeks post-treatment. (g–n) Relative mRNA expression levels of angiogenesis-related genes, including VEGF, HGF, CD31, and vWF, in mouse SG tissues harvested at 1 and 6 weeks post-treatment, as determined by quantitative PCR. Data are presented as mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. ns P > 0.05, ∗ P ≤ 0.05, ∗∗ P ≤ 0.01, and ∗∗∗ P ≤ 0.001.

    Journal: Bioactive Materials

    Article Title: AdMSC spheroids encapsulating antioxidant hybrid protein carrier for irradiation-damaged salivary gland repair

    doi: 10.1016/j.bioactmat.2026.03.049

    Figure Lengend Snippet: Angiogenic effect of spheroids encapsulating GC for IR-damaged salivary glands. (a) Immunofluorescence staining for CD31 (green), an endothelial cell marker, in SG tissue sections to evaluate neovascularization. (b, c) Quantification of CD31-positive areas at 1 and 6 weeks post-treatment. (d) Immunofluorescence staining for VEGF-A (red), an angiogenesis marker, in SG tissue sections. (e, f) Quantification of VEGF-A-positive areas at 1 and 6 weeks post-treatment. (g–n) Relative mRNA expression levels of angiogenesis-related genes, including VEGF, HGF, CD31, and vWF, in mouse SG tissues harvested at 1 and 6 weeks post-treatment, as determined by quantitative PCR. Data are presented as mean ± SD (n = 3). Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. ns P > 0.05, ∗ P ≤ 0.05, ∗∗ P ≤ 0.01, and ∗∗∗ P ≤ 0.001.

    Article Snippet: VEGF and HGF levels were quantified using human VEGF (ABclonal, RK00023) and human HGF ELISA kits according to the manufacturers’ protocols, and absorbance was read at 450 nm with 540 nm reference using a microplate reader (VersaMax; Molecular Devices, USA).

    Techniques: Immunofluorescence, Staining, Marker, Expressing, Real-time Polymerase Chain Reaction

    (A) Expression of KDR, encoding VEGFR2, and (B) FLT4, encoding VEGFR3, across publicly available pediatric solid tumor datasets included in the R2 MegaSampler platform. Expression values are presented as log2-transformed signal intensity. The distributions illustrate inter-dataset and inter-tumor heterogeneity in the expression of receptors associated predominantly with VEGF-A and VEGF-C signaling, respectively. M, metastasis; T, primary tumor; ES, Ewing sarcoma; NB, neuroblastoma; OS, osteosarcoma.

    Journal: bioRxiv

    Article Title: Computationally guided design of a metastasis-on-a-chip platform for quantitative evaluation of chemotactic cues in developmental cancers

    doi: 10.64898/2026.07.25.740695

    Figure Lengend Snippet: (A) Expression of KDR, encoding VEGFR2, and (B) FLT4, encoding VEGFR3, across publicly available pediatric solid tumor datasets included in the R2 MegaSampler platform. Expression values are presented as log2-transformed signal intensity. The distributions illustrate inter-dataset and inter-tumor heterogeneity in the expression of receptors associated predominantly with VEGF-A and VEGF-C signaling, respectively. M, metastasis; T, primary tumor; ES, Ewing sarcoma; NB, neuroblastoma; OS, osteosarcoma.

    Article Snippet: VEGF-A165 and VEGF-C concentrations were quantified using commercially available human ELISA kits (RayBiotech, Peachtree Corners, GA, USA; Catalog Nos.

    Techniques: Expressing, Transformation Assay

    VEGF-C transport was simulated using initial concentrations of 0.1 or 5 µg/mL in Chamber 2. Predicted VEGF-C concentrations over time are shown in (A) Channel 2, adjacent to the source, (B) at the microchannel array separating Reservoirs 2 and 1, and (C) in Channel 1, on the Chamber 1 side of the device. An initial concentration of 5 µg/mL generated measurable exposure at the microchannel array within the experimental time window, whereas 0.1 µg/mL produced substantially lower concentrations and negligible predicted exposure at the microchannel array and in Channel 1. Different concentration units and y-axis ranges were used for the individual device regions.

    Journal: bioRxiv

    Article Title: Computationally guided design of a metastasis-on-a-chip platform for quantitative evaluation of chemotactic cues in developmental cancers

    doi: 10.64898/2026.07.25.740695

    Figure Lengend Snippet: VEGF-C transport was simulated using initial concentrations of 0.1 or 5 µg/mL in Chamber 2. Predicted VEGF-C concentrations over time are shown in (A) Channel 2, adjacent to the source, (B) at the microchannel array separating Reservoirs 2 and 1, and (C) in Channel 1, on the Chamber 1 side of the device. An initial concentration of 5 µg/mL generated measurable exposure at the microchannel array within the experimental time window, whereas 0.1 µg/mL produced substantially lower concentrations and negligible predicted exposure at the microchannel array and in Channel 1. Different concentration units and y-axis ranges were used for the individual device regions.

    Article Snippet: VEGF-A165 and VEGF-C concentrations were quantified using commercially available human ELISA kits (RayBiotech, Peachtree Corners, GA, USA; Catalog Nos.

    Techniques: Concentration Assay, Generated, Produced

    Journal: bioRxiv

    Article Title: Computationally guided design of a metastasis-on-a-chip platform for quantitative evaluation of chemotactic cues in developmental cancers

    doi: 10.64898/2026.07.25.740695

    Figure Lengend Snippet:

    Article Snippet: VEGF-A165 and VEGF-C concentrations were quantified using commercially available human ELISA kits (RayBiotech, Peachtree Corners, GA, USA; Catalog Nos.

    Techniques: Incubation, Cell Culture, Enzyme-linked Immunosorbent Assay

    (A) Representative merged bright-field and fluorescence images of neuroblastoma, Ewing sarcoma, and osteosarcoma cells detected within the microchannel array under control, VEGF-A165, and VEGF-C conditions. Images were processed using a custom Fiji macro that automatically identified the microchannel region, detected fluorescent cells, and retained cells located within the microchannels according to predefined size, circularity, intensity, and channel-overlap criteria. Scale bars =50µm. (B) Quantification of the number of cells detected within the microchannels for neuroblastoma, Ewing sarcoma, and osteosarcoma. Individual data points represent independent microfluidic devices, and bars show mean ± SD. Statistical significance was assessed using ordinary one-way ANOVA followed by Dunnett’s multiple-comparisons test against the corresponding control. *p < 0.05; ns, not significant.

    Journal: bioRxiv

    Article Title: Computationally guided design of a metastasis-on-a-chip platform for quantitative evaluation of chemotactic cues in developmental cancers

    doi: 10.64898/2026.07.25.740695

    Figure Lengend Snippet: (A) Representative merged bright-field and fluorescence images of neuroblastoma, Ewing sarcoma, and osteosarcoma cells detected within the microchannel array under control, VEGF-A165, and VEGF-C conditions. Images were processed using a custom Fiji macro that automatically identified the microchannel region, detected fluorescent cells, and retained cells located within the microchannels according to predefined size, circularity, intensity, and channel-overlap criteria. Scale bars =50µm. (B) Quantification of the number of cells detected within the microchannels for neuroblastoma, Ewing sarcoma, and osteosarcoma. Individual data points represent independent microfluidic devices, and bars show mean ± SD. Statistical significance was assessed using ordinary one-way ANOVA followed by Dunnett’s multiple-comparisons test against the corresponding control. *p < 0.05; ns, not significant.

    Article Snippet: VEGF-A165 and VEGF-C concentrations were quantified using commercially available human ELISA kits (RayBiotech, Peachtree Corners, GA, USA; Catalog Nos.

    Techniques: Fluorescence, Control

    Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing

    doi: 10.1016/j.bioactmat.2026.02.004

    Figure Lengend Snippet: Non-polarised (M0) macrophages grown on CG-155-i scaffolds are driven towards an anti-inflammatory (M2) phenotype. A-B) Assessment of cell viability using metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Gene expression analysis of miRNA-155 and downstream genes demonstrate the activation of anti-inflammatory processes following miRNA-155 inhibition via SHIP1 and SOCS1. F-J) Marker analysis of pro-inflammatory M1 macrophage phenotype (NOS2, CD80, and CD86) and anti-inflammatory M2 phenotype (ARG-1 and CD206) highlight a clear modulation of macrophage polarisation towards an anti-inflammatory state in CG-155-i scaffolds as evidence by decreased NOS2 and CD80 and upregulated ARG1. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Human tumour necrosis factor-alpha (TNF-α, Cat # DY210), interleukin 10 (IL-10, Cat #DY217B), and vascular endothelial growth factor (VEGF, Cat # DY 293B) ELISA kits (R&D Systems, USA) were used to quantify the protein release from cells transfected on miRNA-i-activated scaffolds.

    Techniques: Activity Assay, Gene Expression, Activation Assay, Inhibition, Marker, Expressing

    Pro-inflammatory (M1) macrophages are driven towards an anti-inflammatory (M2) phenotype on CG-155-i scaffolds. A-B) Assessment of cell viability through metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Scaffold-mediated inhibition of miRNA-155 in pro-inflammatory macrophages maintains SHIP1 and SOCS1 upregulation despite the enhanced inflammatory environment. F-H) NOS2 expression shows a trending decrease while CD80 and CD86 levels are downregulated on the CG-155-i scaffolds. I-J) Scaffold-mediated miRNA-155 inhibition does not significantly alter ARG1 expression whereas CD206 is still upregulated, highlighted an M2 macrophage polarisation despite the inflammatory cues. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing

    doi: 10.1016/j.bioactmat.2026.02.004

    Figure Lengend Snippet: Pro-inflammatory (M1) macrophages are driven towards an anti-inflammatory (M2) phenotype on CG-155-i scaffolds. A-B) Assessment of cell viability through metabolic activity and DNA content showed increased macrophage activity and proliferation on the CG-155-i group over 7 days. C-E) Scaffold-mediated inhibition of miRNA-155 in pro-inflammatory macrophages maintains SHIP1 and SOCS1 upregulation despite the enhanced inflammatory environment. F-H) NOS2 expression shows a trending decrease while CD80 and CD86 levels are downregulated on the CG-155-i scaffolds. I-J) Scaffold-mediated miRNA-155 inhibition does not significantly alter ARG1 expression whereas CD206 is still upregulated, highlighted an M2 macrophage polarisation despite the inflammatory cues. K-P) Quantification of TNF-α, IL-10, and VEGF expression at post-transcriptional and post-translational levels further evidences the M2 polarisation of macrophages on CG-155-i scaffolds as shown by IL-10 and VEGF upregulation. Data shows mean ± SD (n = 5), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Human tumour necrosis factor-alpha (TNF-α, Cat # DY210), interleukin 10 (IL-10, Cat #DY217B), and vascular endothelial growth factor (VEGF, Cat # DY 293B) ELISA kits (R&D Systems, USA) were used to quantify the protein release from cells transfected on miRNA-i-activated scaffolds.

    Techniques: Activity Assay, Inhibition, Expressing

    Secretome from macrophages cultured on CG-155-i scaffolds induces anti-inflammatory responses on endothelial cells. A) Cytokine profile analysis revealed an increased release of pro-angiogenic and anti-inflammatory growth factors from macrophages on CG-155-i scaffolds. B-E) Endothelial cells exposed to M0 macrophage secretome show a reduced expression of pro-inflammatory ICAM in the CG-155-i group. F-I) M1 macrophage secretome on endothelial cells elicits clear morphological changes and decreased ICAM intensity in the CG-155-i group. Scale bars = 100 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01.

    Journal: Bioactive Materials

    Article Title: Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing

    doi: 10.1016/j.bioactmat.2026.02.004

    Figure Lengend Snippet: Secretome from macrophages cultured on CG-155-i scaffolds induces anti-inflammatory responses on endothelial cells. A) Cytokine profile analysis revealed an increased release of pro-angiogenic and anti-inflammatory growth factors from macrophages on CG-155-i scaffolds. B-E) Endothelial cells exposed to M0 macrophage secretome show a reduced expression of pro-inflammatory ICAM in the CG-155-i group. F-I) M1 macrophage secretome on endothelial cells elicits clear morphological changes and decreased ICAM intensity in the CG-155-i group. Scale bars = 100 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01.

    Article Snippet: Human tumour necrosis factor-alpha (TNF-α, Cat # DY210), interleukin 10 (IL-10, Cat #DY217B), and vascular endothelial growth factor (VEGF, Cat # DY 293B) ELISA kits (R&D Systems, USA) were used to quantify the protein release from cells transfected on miRNA-i-activated scaffolds.

    Techniques: Cell Culture, Expressing

    Secretome from macrophages on CG-155-i scaffolds enhances endothelial cell migration and organisation into vascular-like structures under chronic-like conditions. A) Endothelial cells exposed to M1 macrophage secretome show reduced migration rates compared to M0 conditions. B-C) Analysis of migration profiles under M0 conditions did not reveal any clear differences in behaviour between treatment groups. D-E) Endothelial cell migration rate exposed to secretome from M1 macrophages on CG-155-i scaffolds result in faster cell migration compared to the negative and miRNA-free groups after 24 h. E) Endothelial cells show higher vascular-like organisation when exposed to M0 macrophage secretome. F-H) Secretome from CG-155-i scaffolds enables improved vascular-like complexity in both M0 and M1 conditions. Scale bars = 500 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p > 0.001, and ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Scaffold-mediated miRNA-155 inhibition promotes regenerative macrophage polarisation leading to anti-inflammatory, angiogenic and neurogenic responses for wound healing

    doi: 10.1016/j.bioactmat.2026.02.004

    Figure Lengend Snippet: Secretome from macrophages on CG-155-i scaffolds enhances endothelial cell migration and organisation into vascular-like structures under chronic-like conditions. A) Endothelial cells exposed to M1 macrophage secretome show reduced migration rates compared to M0 conditions. B-C) Analysis of migration profiles under M0 conditions did not reveal any clear differences in behaviour between treatment groups. D-E) Endothelial cell migration rate exposed to secretome from M1 macrophages on CG-155-i scaffolds result in faster cell migration compared to the negative and miRNA-free groups after 24 h. E) Endothelial cells show higher vascular-like organisation when exposed to M0 macrophage secretome. F-H) Secretome from CG-155-i scaffolds enables improved vascular-like complexity in both M0 and M1 conditions. Scale bars = 500 μm. Data shows mean ± SD (n = 4), ∗ indicates p < 0.05, ∗∗p < 0.01, ∗∗∗p > 0.001, and ∗∗∗∗p < 0.0001.

    Article Snippet: Human tumour necrosis factor-alpha (TNF-α, Cat # DY210), interleukin 10 (IL-10, Cat #DY217B), and vascular endothelial growth factor (VEGF, Cat # DY 293B) ELISA kits (R&D Systems, USA) were used to quantify the protein release from cells transfected on miRNA-i-activated scaffolds.

    Techniques: Migration