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: iMeta

Article Title: Dissecting the angiogenic mechanism of pachychoroid polypoidal choroidal vasculopathy

doi: 10.1002/imt2.70176

Figure Lengend Snippet: Effects of OSS on mCECs following Edn1 knockdown and re‐expression and Ednra knockdown. (A) Representative immunofluorescence images of F‐actin and VE‐cadherin. F‐actin length and VE‐cadherin fluorescence intensity were quantified using ImageJ (version 1.54p). n = 3 independent biological replicates per group. (B) Potential targets for single‐cell sequencing based on qRT‐PCR screening. n = 3 independent biological replicates per group. (C) Representative trajectories of mCECs under laminar flows shear stress and oscillatory flow shear stress with and without Edn1 shRNA. The change in displacement in 24 h was determined for each experiment and used as a single data point ( n = 3 independent biological replicates per group). (D) CCK8‐based proliferation and transwell‐based invasion assays assessing the effects of OSS and Edn1 knockdown. Edn1 silencing significantly attenuated the OSS‐induced reduction in proliferation and increase in invasion of mCECs. n = 5 independent biological replicates. (E) Tube formation of mCECs under OSS with or without Edn1 knockdown. OSS promoted tube formation, whereas Edn1 knockdown attenuated this effect. The number of master junctions and total branching length were quantified using ImageJ, n = 3 independent biological replicates. (F) Representative Western blots showing the expression of EDN1, c‐Casp3, ANG‐1, MMP9, IL‐6, and ZO‐1 in response to OSS with and without Edn1 shRNA. n = 3 independent biological replicates. (G) CCK8 assays of mCEC proliferation under OSS following Edn1 re‐expression after Edn1 knockdown. n = 5 independent biological replicates. Transwell invasion (H) and scratch migration (I) assays showing that the OSS‐induced invasive and migratory responses of mCEC cells were attenuated by Edn1 knockdown and restored by Edn1 re‐expression. n = 5 independent biological replicates per group for the Transwell invasion assay and n = 3 for the scratch migration assay. (J) Representative fluorescence images of ROS production in mCECs exposed to OSS following Edn1 knockdown and/or re‐expression. Intracellular ROS levels were assessed by DCF fluorescence. n = 3 independent biological replicates per group. (K) Expression of EDN1, c‐Casp3, ANG‐1, MMP9, IL‐6, and ZO‐1 following Edn1 knockdown and subsequent Edn1 re‐expression. n = 3 independent biological replicates per group. (L) Co‐immunoprecipitation showing the interaction between EDN1 and EDNRA in mCECs protein extracts. n = 3 independent biological replicates. (M) Representative trajectories of mCECs exposed to OSS with or without Ednra knockdown. The change in displacement over 24 h was calculated for each independent experiment. n = 3 independent biological replicates per group. (N) CCK8 assay assessing the effects of OSS and Ednra knockdown on mCEC proliferation. Ednra silencing significantly attenuated the OSS‐induced reduction in proliferation. n = 5 independent biological replicates per group. Scratch migration (O) and Transwell invasion (P) assays showing that OSS increased the migratory and invasive capacities of mCECs and that these effects were attenuated by Ednra knockdown. n = 3 independent biological experiments for the scratch migration assay and n = 5 for the transwell invasion assay. (Q) Ednra silencing reduced the expression of EDNRA, c‐Casp3, ANG‐1, MMP9, and IL‐6 and increased ZO‐1 expression. n = 3 independent biological replicates per group. OSS, oscillatory shear stress (±6 dyn/cm 2 , 12 h); CN, control (laminar shear stress at 6 dyn/cm 2 ); shEdn1, Edn1 shRNA, oeEdn1, over‐expressed Edn1 ; shEdnra, Ednra shRNA; qRT‐PCR, quantitative reverse transcription polymerase chain reaction; CCK‐8, Cell Counting Kit‐8; DCF, dichlorofluorescein; IP, immunoprecipitation; IgG, immunoglobulin G; ROS, reactive oxygen species. Data are presented as mean ± SD from n independent biological replicates. For two‐group comparisons, statistical significance was assessed by two‐tailed unpaired Student's t ‐test; for multiple groups, by one‐way ANOVA followed by Tukey's multiple comparisons test. Independent biological replicates: separate cell‐culture experiments per condition. The single and double asterisks indicate p < 0.05 and p < 0.01, respectively.

Article Snippet: Primary antibodies against EDN1 (Abcam, Cat. No. ab117757), EDNRA (Abcam, Cat. No. ab117521), MMP9 (Santa Cruz, Cat. No. sc‐393859), IL‐6 (HUABIO, Hangzhou, HA601051 ), ZO‐1 (Cell Signaling, Cat. No.13663), c‐Casp3 (Cell Signaling, Cat. No.9661), angiopoietin 1 (HUABIO, Hangzhou, Cat. No. ET1611‐28), and β‐actin (Sigma, Cat. No. A5441) were used.

Techniques: Knockdown, Expressing, Immunofluorescence, Fluorescence, Single-Cell Sequencing, Quantitative RT-PCR, Screening, Shear, shRNA, Western Blot, Migration, Transwell Invasion Assay, Co-Immunoprecipitation Assay, CCK-8 Assay, Control, Reverse Transcription, Polymerase Chain Reaction, Cell Counting, Immunoprecipitation, Two Tailed Test, Cell Culture

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