Journal: Materials Today Bio

Article Title: Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling

doi: 10.1016/j.mtbio.2026.103564

Figure Lengend Snippet: In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Article Snippet: Proliferation and remodeling markers: PCNA (1:1000, ab29, Abcam), IL-6 (1:1000, A0286, ABclonal), TGF-β1 (1:1000, A2124, ABclonal), MMP-2 (1:1000, A6247, ABclonal), and MMP-9 (1:1000, A2095, ABclonal).

Techniques: In Vivo, Inhibition, Disruption, Staining, Expressing, Marker

Journal: Biomaterials Research

Article Title: A Glucose-Responsive Hydrogel with Multifunctional Properties for Accelerated Diabetic Wound Healing

doi: 10.34133/bmr.0405

Figure Lengend Snippet: The synthesis process of phenylboronic-acid-functionalized oxidized sodium alginate and gallic-acid-conjugated chitosan (OSA-PBA/CS-GA) hydrogel and its multifunctional mechanisms in healing diabetic wounds. ROS, reactive oxygen species; SOD, superoxide dismutase; CAT, catalase; MDA, malondialdehyde; α-SMA, alpha smooth muscle actin; VEGF, vascular endothelial growth factor; IL-6, interleukin 6; MMP9, matrix metalloproteinase 9.

Article Snippet: Sections were incubated overnight at 4 °C with primary antibodies including matrix metalloproteinase 9 (MMP9; A0289), interleukin-6 (IL-6; A21264) (ABclonal, China), CD86 (30691-1-AP), CD206 (18704-1-AP) (Proteintech), CD31 (ab281583), vascular endothelial growth factor (VEGF; ab32152) (Abcam, UK), and alpha smooth muscle actin (α-SMA; A2235, ABclonal).

Techniques:

Journal: Science Advances

Article Title: Loading is not delivering: Intracellular drug retention and migration capacity govern macrophage-based drug delivery

doi: 10.1126/sciadv.aec0429

Figure Lengend Snippet: ( A ) GO enrichment analysis ( q < 0.0001) of differentially expressed genes in particle-loaded macrophages (PLGA0.2@MΦ, PLGA1@MΦ, and PLGA3@MΦ), each compared to untreated macrophages (MΦ). ( B ) Quantification of intracellular ROS by mean fluorescence intensity (MFI) in particle-loaded macrophages (PLGA0.2@MΦ, PLGA1@MΦ, and PLGA3@MΦ), normalized to untreated macrophages (MΦ) ( n = 6). ( C ) KEGG pathway enrichment analysis ( q < 0.01) of differentially expressed genes in particle-loaded macrophages (PLGA0.2@MΦ, PLGA1@MΦ, and PLGA3@MΦ), each compared to untreated macrophages (MΦ). ( D ) Quantitative PCR analysis of migration- and cytoskeleton-related genes, including SOCS3, PUMA, BCL2L1, CXCR4, ITGB1, MMP9, and MYL9. ( E ) Representative Western blot images of MMP9 and phosphorylated Akt (P-Akt). ( F and G ) Relative expression of CXCR4 (F) and ITGB1 (G) (flow cytometry, n = 3). ( H ) Chemotactic migration of macrophages in the presence of NAC ( n = 5). ( I ) Schematic illustration of the mechanisms by which nanoparticles impair the migratory capacity of carrier macrophages. Created in BioRender. Huang, Y. (2026) https://BioRender.com/8j9iroe . ** P < 0.01 and **** P < 0.0001; the data are shown as mean ± SD, statistical significance was analyzed using a one-way ANOVA with Tukey’s multiple comparisons [(B) and (F) to (H)].

Article Snippet: After blocking with a protein-free rapid blocking buffer (Epizyme Biotech, catalog no. PS108), the membranes were incubated overnight at 4°C with primary antibodies targeting P-Akt (Cell Signaling Technology, catalog no. 4060, lot no. 27), MMP9 (ABclonal Technology, catalog no. A0289, lot no. 1151690201), and GAPDH (Servicebio, catalog no. ZB15004-HRP, lot no. AC251027003) as the loading control.

Techniques: Fluorescence, Real-time Polymerase Chain Reaction, Migration, Western Blot, Expressing, Flow Cytometry