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vascular endothelial growth factor  (R&D Systems)


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    Structured Review

    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 433 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vascular+endothelial+growth+factor/Human+VEGF+DuoSet+ELISA/pmc12926579-106-14-25
    Average 96 stars, based on 433 article reviews
    vascular endothelial growth factor - by Bioz Stars, 2026-09
    96/100 stars

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    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

    Related Articles

    Derivative Assay:

    Article Title: Inflammatory Mediators Both Directly and Indirectly Promote Microglial Proliferation.
    Article Snippet: .. We tested the following factors: nerve growth factor β (βNGF; Gibco 450–34), brain derived neurotrophic factor (BDNF; Gibco 450–02), colony stimulating factor- 3 (CSF3; Gibco AF- 250- 05), fractalkine (CX3CL1; Gibco 300–31), interferon- ɣ (IFNɣ; ThermoFisher Scientific BMS326), insulin- like growth factor 1 (IGF1; Gibco 250–19), interleukin- 17A (IL17A; Gibco 210- 17), interleukin- 1ɑ (IL1ɑ; R&D Systems 400- ML- 005), interleukin- 1β (IL1β; R&D Systems 401- ML- 005), interleukin- 33 (IL33; Gibco 210–33), interleukin- 4 (IL4; Gibco 214–14), interleukin- 5 (IL5; Gibco 215–15), lysophosphatidic acid (LPA; Sigma Aldrich 857128P), neurotensin (NTS; R&D Systems 1909), neuregulin- 1 (NRG1; Gibco 100–03), pleiotrophin (PTN; R&D Systems 6580- PL), stem cell factor (SCF; Gibco 250–03), sphingosine- 1- phosphate (S1P; R&D Systems 1370), vascular endothelial growth factor (VEGF; R&D Systems 493- MV- 005), and Wnt family member 3a (WNT3A; Gibco 315–20). ..

    Article Title: Inflammatory Mediators Both Directly and Indirectly Promote Microglial Proliferation
    Article Snippet: .. We tested the following factors: nerve growth factor β (βNGF; Gibco 450–34), brain derived neurotrophic factor (BDNF; Gibco 450–02), colony stimulating factor‐3 (CSF3; Gibco AF‐250‐05), fractalkine (CX3CL1; Gibco 300–31), interferon‐ɣ (IFNɣ; ThermoFisher Scientific BMS326), insulin‐like growth factor 1 (IGF1; Gibco 250–19), interleukin‐17A (IL17A; Gibco 210‐17), interleukin‐1ɑ (IL1ɑ; R&D Systems 400‐ML‐005), interleukin‐1β (IL1β; R&D Systems 401‐ML‐005), interleukin‐33 (IL33; Gibco 210–33), interleukin‐4 (IL4; Gibco 214–14), interleukin‐5 (IL5; Gibco 215–15), lysophosphatidic acid (LPA; Sigma Aldrich 857128P), neurotensin (NTS; R&D Systems 1909), neuregulin‐1 (NRG1; Gibco 100–03), pleiotrophin (PTN; R&D Systems 6580‐PL), stem cell factor (SCF; Gibco 250–03), sphingosine‐1‐phosphate (S1P; R&D Systems 1370), vascular endothelial growth factor (VEGF; R&D Systems 493‐MV‐005), and Wnt family member 3a (WNT3A; Gibco 315–20). ..

    Enzyme-linked Immunosorbent Assay:

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

    Article Title: Nicotine-free electronic vape fluid stimulates angiogenic processes in vitro through ARF6-mediated oxidative stress
    Article Snippet: Antibodies against β-actin (Ab8227), 2′,7′-dichlorofluorescein diacetate (DCFDA; Ab145286 ), and assay kits for superoxide dismutase (SOD; Ab65354), catalase (CAT; Ab83464), and glutathione peroxidase (GSH-Px; Ab102530 ) were purchased from Abcam (Cambridge, UK). .. NAV2729 and Secin H3 were purchased from Tocris Bioscience (Abingdon, UK); Proteome Profiler Human angiogenesis array and enzyme-linked immunosorbent assay (ELISA) kits for human angiopoietin-2 (DANG20), endothelial growth factor (EGF; DEG00), endoglin (DNDG00), placental growth factor (PIGF; DPG00), prolactin (DY682), and vascular endothelial growth factor (VEGF; DVE00) were all obtained from R&D Systems (Abingdon, UK). ..

    Transfection:

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

    Cell Culture:

    Article Title: Directly reprogrammed NK cells driven by BCL11B depletion enhance targeted immunotherapy against pancreatic ductal adenocarcinoma
    Article Snippet: Briefly, cells were dissociated into single-cell suspensions using TrypLE Express (Thermo Fisher Scientific) at 37 °C and passed through a 70 μm cell strainer. .. A total of 8 × 10 3 cells were seeded into each well of a round-bottom 96-well plate, centrifuged at 1,500 rpm for 4 min at 8 °C, and cultured in STEMdiffTM APELTM2 Medium (STEMCELL Technologies) supplemented with 40 ng/mL SCF, vascular endothelial growth factor (VEGF; R&D Systems), and 20 ng/mL bone morphogenetic protein 4 (BMP4; PeproTech) at 37 °C for 6 days. .. To initiate NK lineage differentiation, 6–8 spin EBs were transferred into each well of a 2% gelatin-coated 24-well plate and cultured in NK cell differentiation medium (NKM), composed of 56.6% DMEM, 28.3% Ham’s F-12, 15% human AB serum (Sigma), 5 ng/mL sodium selenite (Sigma), 50 μM ethanolamine (Sigma), 20 μg/mL ascorbic acid, 25 μM β-mercaptoethanol, 2 mM L-glutamine, and 1% P/S.

    Article Title: Directly reprogrammed NK cells driven by BCL11B depletion enhance targeted immunotherapy against pancreatic ductal adenocarcinoma.
    Article Snippet: Briefly, cells were dissociated into single-cell suspensions using TrypLE Express (Thermo Fisher Scientific) at 37 °C and passed through a 70 μm cell strainer. .. A total of 8 × 103 cells were seeded into each well of a round-bottom 96-well plate, centrifuged at 1,500 rpm for 4 min at 8 °C, and cultured in STEMdiffTM APELTM2 Medium (STEMCELL Technologies) supplemented with 40 ng/mL SCF, vascular endothelial growth factor (VEGF; R&D Systems), and 20 ng/ mL bone morphogenetic protein 4 (BMP4; PeproTech) at 37 °C for 6 days. .. To initiate NK lineage differentiation, 6–8 spin EBs were transferred into each well of a 2% gelatin-coated 24-well plate and cultured in NK cell differentiation medium (NKM), composed of 56.6% DMEM, 28.3% Ham’s F-12, 15% human AB serum (Sigma), 5 ng/mL sodium selenite (Sigma), 50 μM ethanolamine (Sigma), 20 μg/mL ascorbic acid, 25 μM β-mercaptoethanol, 2 mM L-glutamine, and 1% P/S.



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    Temporal analysis of the BMSC paracrine profile on different scaffolds. (A) Confocal microscopy images from Live/Dead fluorescence staining of BMSCs encapsulated within the PCL/HAp-GelMA/BMSCs scaffold after 1, 3, 5, and 14 d of 3D culture (live cells, green; dead cells, red). (B) The concentrations of key paracrine factors (TGF-β, PGE2, VEGF, HGF, and BMP-2) from BMSCs cultured in different scaffolds, quantified from culture supernatants at day 3 and day 7. (C) Corresponding relative mRNA expression levels of TGFB1, PTGS2, VEGFA, HGF, and BMP-2 in BMSCs at day 3 and day 7, as determined by qPCR analysis. Data are presented as mean ± SD (n = 3) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns: not significant.

    Journal: Bioactive Materials

    Article Title: Mesenchymal stromal cells-loaded 3D radially aligned composite scaffold with potentiated paracrine signaling for sequential bone regeneration

    doi: 10.1016/j.bioactmat.2026.02.059

    Figure Lengend Snippet: Temporal analysis of the BMSC paracrine profile on different scaffolds. (A) Confocal microscopy images from Live/Dead fluorescence staining of BMSCs encapsulated within the PCL/HAp-GelMA/BMSCs scaffold after 1, 3, 5, and 14 d of 3D culture (live cells, green; dead cells, red). (B) The concentrations of key paracrine factors (TGF-β, PGE2, VEGF, HGF, and BMP-2) from BMSCs cultured in different scaffolds, quantified from culture supernatants at day 3 and day 7. (C) Corresponding relative mRNA expression levels of TGFB1, PTGS2, VEGFA, HGF, and BMP-2 in BMSCs at day 3 and day 7, as determined by qPCR analysis. Data are presented as mean ± SD (n = 3) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns: not significant.

    Article Snippet: ELISA kits for PGE2 (Cat. No. E-EL-0034), TGF-β (Cat. No. E-EL-0162), VEGF (Cat. No. E-EL-R2603), and HGF (Cat. No. E-EL-R0496) were purchased from Elabscience (Wuhan, China).

    Techniques: Confocal Microscopy, Fluorescence, Staining, Cell Culture, Expressing

    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

    Schematic illustration of the a) preparation and application of Ti-OH-ePV; b) VEGF release of Ti-OH-ePV under different pH conditions; c) anastomotic healing performance with Ti and Ti-OH-ePV; d) healing-promotion mechanism of Ti-OH-ePV.

    Journal: Bioactive Materials

    Article Title: Bioactive-coated porous anastomotic staples enhance anastomotic healing

    doi: 10.1016/j.bioactmat.2026.01.005

    Figure Lengend Snippet: Schematic illustration of the a) preparation and application of Ti-OH-ePV; b) VEGF release of Ti-OH-ePV under different pH conditions; c) anastomotic healing performance with Ti and Ti-OH-ePV; d) healing-promotion mechanism of Ti-OH-ePV.

    Article Snippet: Vascular Endothelial Growth Factor (VEGF) protein was supplied by MedChemExpress LLC (USA).

    Techniques:

    Structure characterization of Ti-OH-ePV. a) SEM images of Ti, Ti-OH, and Ti-OH-ePV (scale bars: 1 μm); b) Elemental mapping of Ti-OH-ePV; c) CV test of DA and VEGF solution under a nitrogen atmosphere; d) AFM height images of Ti, Ti-OH, and Ti-OH-ePV; e) Surface Sa (arithmetic mean height) via AFM of Ti, Ti-OH, and Ti-OH-ePV; f) Water contact angle of Ti, Ti-OH, and Ti-OH-ePV; g) FTIR spectra of Ti, Ti-OH, and Ti-OH-ePV; h) Tensile testing of the Ti, Ti-OH, and Ti-OH-ePV; i) Single anastomotic staple tensile strength testing of the Ti, Ti-OH, and Ti-OH-ePV; j) VEGF release profiles of the Ti-OH-ePV, Ti-ePV, and Ti-OH-PV in buffer solutions at pH = 7.4; k) VEGF release profiles of the Ti-OH-ePV, Ti-ePV, and Ti-OH-PV in buffer solutions at pH = 6.5; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Bioactive Materials

    Article Title: Bioactive-coated porous anastomotic staples enhance anastomotic healing

    doi: 10.1016/j.bioactmat.2026.01.005

    Figure Lengend Snippet: Structure characterization of Ti-OH-ePV. a) SEM images of Ti, Ti-OH, and Ti-OH-ePV (scale bars: 1 μm); b) Elemental mapping of Ti-OH-ePV; c) CV test of DA and VEGF solution under a nitrogen atmosphere; d) AFM height images of Ti, Ti-OH, and Ti-OH-ePV; e) Surface Sa (arithmetic mean height) via AFM of Ti, Ti-OH, and Ti-OH-ePV; f) Water contact angle of Ti, Ti-OH, and Ti-OH-ePV; g) FTIR spectra of Ti, Ti-OH, and Ti-OH-ePV; h) Tensile testing of the Ti, Ti-OH, and Ti-OH-ePV; i) Single anastomotic staple tensile strength testing of the Ti, Ti-OH, and Ti-OH-ePV; j) VEGF release profiles of the Ti-OH-ePV, Ti-ePV, and Ti-OH-PV in buffer solutions at pH = 7.4; k) VEGF release profiles of the Ti-OH-ePV, Ti-ePV, and Ti-OH-PV in buffer solutions at pH = 6.5; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Vascular Endothelial Growth Factor (VEGF) protein was supplied by MedChemExpress LLC (USA).

    Techniques:

    a) The procedure of gastrointestinal anastomosis in New Zealand rabbit; b) Immumohistochemical staining images of IL-6, TNF-α, TGF-β, and IL-10 at the anastomotic stoma on day 3 for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 25 μm); c) Statistical analysis of IL-6 expression in different groups; d) Statistical analysis of TNF-α expression in different groups; e) Statistical analysis of TGF-β expression in different groups; f) Statistical analysis of IL-10 expression in different groups; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Bioactive Materials

    Article Title: Bioactive-coated porous anastomotic staples enhance anastomotic healing

    doi: 10.1016/j.bioactmat.2026.01.005

    Figure Lengend Snippet: a) The procedure of gastrointestinal anastomosis in New Zealand rabbit; b) Immumohistochemical staining images of IL-6, TNF-α, TGF-β, and IL-10 at the anastomotic stoma on day 3 for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 25 μm); c) Statistical analysis of IL-6 expression in different groups; d) Statistical analysis of TNF-α expression in different groups; e) Statistical analysis of TGF-β expression in different groups; f) Statistical analysis of IL-10 expression in different groups; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Vascular Endothelial Growth Factor (VEGF) protein was supplied by MedChemExpress LLC (USA).

    Techniques: Staining, Expressing

    a) Immumohistochemical staining images of CD31 on day 7 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 25 μm); b) Masson staining images on day 14 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 20 μm); c) H&E staining images on day 14 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups; d) Statistical analysis for the number of blood vessels in different groups; e) Statistical analysis of collagen expression in different groups; f) Statistical analysis of bursting pressure on days 7, and 14 in different groups; g) Statistical analysis of WBC on days pre-1, 3, 7, and 14 in different groups; h) Statistical analysis of APTT on days pre-1, 3, 7, and 14 in different groups; i) Statistical analysis of ALT on days pre-1, 3, 7, and 14 in different groups; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Bioactive Materials

    Article Title: Bioactive-coated porous anastomotic staples enhance anastomotic healing

    doi: 10.1016/j.bioactmat.2026.01.005

    Figure Lengend Snippet: a) Immumohistochemical staining images of CD31 on day 7 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 25 μm); b) Masson staining images on day 14 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups (scale bar: 20 μm); c) H&E staining images on day 14 at the anastomotic stoma for Ti, Ti-OH, Ti-OH-ePDA (PDA-only), and Ti-OH-ePV (VEGF-loaded PDA) groups; d) Statistical analysis for the number of blood vessels in different groups; e) Statistical analysis of collagen expression in different groups; f) Statistical analysis of bursting pressure on days 7, and 14 in different groups; g) Statistical analysis of WBC on days pre-1, 3, 7, and 14 in different groups; h) Statistical analysis of APTT on days pre-1, 3, 7, and 14 in different groups; i) Statistical analysis of ALT on days pre-1, 3, 7, and 14 in different groups; n = 3; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: Vascular Endothelial Growth Factor (VEGF) protein was supplied by MedChemExpress LLC (USA).

    Techniques: Staining, Expressing