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94
ATCC cow pulmonary artery endothelial
Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote <t>endothelial</t> differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.
Cow Pulmonary Artery Endothelial, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
PromoCell endothelial growth medium
Cytocompatibility of Cu-PIAS. ( A ) Viability, as measured by ATP content, of human umbilical vein <t>endothelial</t> cells cultured with media containing extracts of 15-Cu-PIAS, Latex (Positive), or PCL (Negative) over three days. ( B ) Representative images of cell morphology after 24 h exposure to material extract-containing media, visualized by Calcein AM (Green) staining. Additional staining with ethidium homodimer-1 (red) indicates the presence of non-viable cells.
Endothelial Growth Medium, supplied by PromoCell, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Elabscience Biotechnology vegf
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.
Vegf, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
PromoCell hydrocortisone
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.
Hydrocortisone, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
PromoCell cell growth medium 2
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.
Cell Growth Medium 2, supplied by PromoCell, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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86
Procell Inc mouse coronary artery endothelial cells mcaecs
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.
Mouse Coronary Artery Endothelial Cells Mcaecs, supplied by Procell 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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86
Applied Biological Materials Inc mouse liver sinusoidal endothelial cells
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.
Mouse Liver Sinusoidal Endothelial Cells, supplied by Applied Biological Materials 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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huvecs  (ATCC)
99
ATCC huvecs
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.
Huvecs, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC endothelial cell line ea hy926
Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation <t>assay.</t> <t>EA.hy926</t> cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.
Endothelial Cell Line Ea Hy926, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.

Journal: Bioactive Materials

Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

doi: 10.1016/j.bioactmat.2026.03.040

Figure Lengend Snippet: Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.

Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

Techniques: Construct

in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.

Journal: Bioactive Materials

Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

doi: 10.1016/j.bioactmat.2026.03.040

Figure Lengend Snippet: in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.

Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

Techniques: In Vitro, MTT Assay, Staining, Control, Viability Assay

rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.

Journal: Bioactive Materials

Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

doi: 10.1016/j.bioactmat.2026.03.040

Figure Lengend Snippet: rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.

Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

Techniques: Activation Assay, RNA Sequencing, Cell Differentiation

Cytocompatibility of Cu-PIAS. ( A ) Viability, as measured by ATP content, of human umbilical vein endothelial cells cultured with media containing extracts of 15-Cu-PIAS, Latex (Positive), or PCL (Negative) over three days. ( B ) Representative images of cell morphology after 24 h exposure to material extract-containing media, visualized by Calcein AM (Green) staining. Additional staining with ethidium homodimer-1 (red) indicates the presence of non-viable cells.

Journal: Bioactive Materials

Article Title: A catalytically active and recyclable bioelastomer inspired by metalloenzymes

doi: 10.1016/j.bioactmat.2026.02.053

Figure Lengend Snippet: Cytocompatibility of Cu-PIAS. ( A ) Viability, as measured by ATP content, of human umbilical vein endothelial cells cultured with media containing extracts of 15-Cu-PIAS, Latex (Positive), or PCL (Negative) over three days. ( B ) Representative images of cell morphology after 24 h exposure to material extract-containing media, visualized by Calcein AM (Green) staining. Additional staining with ethidium homodimer-1 (red) indicates the presence of non-viable cells.

Article Snippet: Briefly, endothelial growth medium supplemented with 5% fetal bovine serum, growth factors, ascorbic acid, and hydrocortisone (Promocell C-22121) was incubated at 37 °C for 72 h under agitation alone, or in the presence of 15-Cu-PIAS (6 cm 2 /mL), PCL (6 cm 2 /mL), or latex (3 cm 2 /mL) sheets cut into several 6 mm × 6 mm squares.

Techniques: Cell Culture, Staining

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

Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation assay. EA.hy926 cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.

Journal: Tumour Virus Research

Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth

doi: 10.1016/j.tvr.2026.200340

Figure Lengend Snippet: Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation assay. EA.hy926 cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.

Article Snippet: Human hepatoma cell lines HepG2 (ATCC, HB–8065) and Huh7 (JCRB, JCRB0403), endothelial cell line EA.hy926 (ATCC, CRL–2922TM), and HEK293T cells (ATCC, CRL–3216) were obtained from the American Type Culture Collection (ATCC) and the Japanese Collection of Research Bioresources Cell Bank (JCRB, Japan).

Techniques: Expressing, Stable Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Endothelial Tube Formation Assay, Cell Culture, Transwell Migration Assay, Migration, Derivative Assay, Immunohistochemical staining, Staining