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

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

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

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

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: The supernatants were collected from cells, and VEGFA was quantified by using the Human VEGF/VEGFA ELISA Kit (Boster, # EK0539).

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