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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, <t>VEGF,</t> 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.
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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, <t>VEGF,</t> 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.
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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.
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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.
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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.
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Image Search Results


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