cd31  (R&D Systems)

Journal: Bioactive Materials

Article Title: Injection site dictates the immune response to a biodegradable polymer and corresponding collagen regeneration

doi: 10.1016/j.bioactmat.2026.04.004

Figure Lengend Snippet: ID tissue exhibits higher densities of fibroblasts, macrophages, and microvessels compared to SC tissue. Immunofluorescence analysis comparing the expression of Vimentin (a fibroblast marker), CD68 (a macrophage marker), and CD31 (an endothelial cell marker) in ID and SC tissues. For each group, n = 3; data represent mean ± s.d.; ∗P < 0.05 and ∗∗P < 0.01.

Article Snippet: After antigen retrieval and blocking, sections were incubated overnight at 4 °C with primary antibodies targeting vimentin, CD68 (ABclonal, A20803), CD31 (R&D SYSTEMS, AF3628), HMGB1 (Cell Signaling Technology, 3935), HSP70 (ABclonal, A23457), NF-κB p65 (ABclonal, A19653), CD206 (Cell Signaling Technology, 24595), and FAPα (ABclonal, A23789 ).

Techniques: Immunofluorescence, Expressing, Marker

Journal: Bioactive Materials

Article Title: Glucose/ROS-responsive and redox-gated adaptive hydrogel dressing for accelerating diabetic wound repair via synergistic cGAS/STING pathway inhibition and oxidative stress alleviation

doi: 10.1016/j.bioactmat.2026.03.025

Figure Lengend Snippet: The cellular uptake and anti-inflammatory effect of HPSL in vitro . (A) Flow cytometry analysis and (B) semi-quantitative analysis of cellular uptake of PSL and blank NPs by M1 macrophages. n = 3. (C) Representative Giemsa staining images of LPS and high glucose-stimulated RAW 264.7 cells with different formulations, scale bar = 50 μm. (D) Immunofluorescence staining and semi-quantitative analysis of CD68 (red) and iNOS (green) in RAW 264.7 cells from different treatment groups, scale bar = 50 μm. n = 6. (E) Immunofluorescence staining and semi-quantitative analysis of CD68 (green) and Arg-1 (red) in RAW 264.7 cells from different treatment groups, scale bar = 50 μm. n = 6. Western blotting analysis and corresponding semi-quantitative analysis of (F) STING/ p -STING, (G) TBK1/ p -TBK1, (H) IRF3/ p -IRF3, (I) NF-κB, (J) TNF-α, and (K) IL-6, Lane 1: Normal group, Lane 2: Model group, Lane 3: PSL group, Lane 4: Free H151 group, Lane 5: HPSL group. n = 3. All data are shown as mean ± SEM.

Article Snippet: CD68-specific antibodies were purchased from Proteintech Group, Inc. (Wuhan, China).

Techniques: In Vitro, Flow Cytometry, Staining, Immunofluorescence, Western Blot

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: Schematic illustration of PTR-SeNPs and MUC1@PTR-SeNPs synthesis and their anti-tumor efficacy against human triple-negative breast cancer.

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques:

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: Structure characterization of PTR-SeNPs and MUC1@ PTR-SeNPs. Structure characterization of PTR-SeNPs by (A) TEM, (B) Zetasizer Nano ZS, (C, D) Nanosight NS300, (E1-4) HRTEM-EDS and (F, G) FT-IR. (H) Confirmation of MUC1-C + PTR-SeNPs conjugation by confocal microscopy after fluorescent labeling with anti-mouse IgG (H + L). (I, J) Characterization results of the particle size and potential of MUC1@PTR-SeNPs

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: Conjugation Assay, Confocal Microscopy, Labeling

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: In vitro anti-tumor efficacy of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC c ell lines. ( A, B ) Protein expression level of MUC1 in 17 different TNBC cell lines. ( C, D ) IC 50 and maximum % growth inhibition of PTR-SeNPs and MUC1@PTR-SeNPs on 17 TNBC cell lines. ( E, G ) Cell cycle distribution triggered by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with PTR-SeNPs or MUC1@PTR-SeNPs (4 and 40 μM) in HCC1937 and MDA-MB-436 cells for 72 h, cells were stained with propidium iodide followed by flow cytometry analysis using MultiCycle software. The apoptotic cell death was quantified by measuring the sub-G1 cell population. ( F, H ) Phosphatidylserine translocation mediated by PTR-SeNPs and MUC1@PTR-SeNPs in HCC1937 and MDA-MB-436 cells. After treatment with MUC1@PTR-SeNPs (4 and 40 μM) for 48 h, cells were co-stained with propidium iodide and Annexin-V-FITC followed by flow cytometry analysis [early apoptotic subset: Annexin V+/PI- (green); late apoptotic subset: Annexin V+/PT+ (red)].

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: In Vitro, Expressing, Inhibition, Staining, Flow Cytometry, Software, Translocation Assay

Journal: Bioactive Materials

Article Title: Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway

doi: 10.1016/j.bioactmat.2026.02.027

Figure Lengend Snippet: In vivo anti-tumor efficacy of MUC1@PTR- SeNPs. (A) MUC1 mRNA expression in normal tissue and primary breast cancer tumor using GEPIA database. ( B ) MUC1 expression in tumor tissues of MDA-MB-468-bearing mice in preliminary study. (C – E) Dose-dependent study of tumor inhibition effect of MUC1@PTR-SeNPs [75 (Low), 375 (Mid) & 750 μg (High) Se/kg BW/day] on BALB/c nude mice transplanted with MDA-MB-468 xenograft after oral administration for 30 days. PTR-SeNPs (High; 750 μg Se/kg BW/day) was used to investigate the possible improvement of in vivo anti-tumor efficacy by the MUC1@PTR-SeNPs. Quantitative analysis of Se content (μg/g) in (F) blood and (G) tumor tissue of experimental mice. (H) H&E, Ki67 and Tunnel fluorescence staining of tumor sections to detect apoptosis in vivo . (I) Western blot analysis of PARP, p-Bcl-2, Bax and C-caspase-9 protein expression in tumor sections. (J) In the serum of each group of tumor-bearing mice, the results of blood biochemistry-related indexes were analyzed.

Article Snippet: Anti-human MUC1 therapeutic antibody Fab fragment (7B8) were purchased From Creative Biolabs (TAB-423MZ-F, USA).

Techniques: In Vivo, Expressing, Inhibition, Fluorescence, Staining, Western Blot

Journal: Bioactive Materials

Article Title: Skin-mimetic bilayer hydrogel normalizes diabetic wound healing by orchestrating inflammatory cell dynamics: An early intervention strategy

doi: 10.1016/j.bioactmat.2026.02.025

Figure Lengend Snippet: In vitro assay of inflammation cell modulation under stimulation of SP-loaded Gel/HA and IL-10-loaded Ker/Cu. a Schematic of neutrophil migration test using a transwell system after treatment with the leaching solution of SP@Gel/HA. Gel/HA and blank culture medium were set for comparison. b Wright-Giemsa staining of HL-60 cells before and after differentiation. c Photograph of dHL-60 cells migrating to the lower chamber. d Quantitative analysis of neutrophil migration after treatments with SP@Gel/HA and Gel/HA. Untreated group serves as a control. e Schematic of macrophage polarization after treatment with LPS, IL-10, or IL-10/LPS. f Representative fluorescence images of macrophages after different treatment. Red: iNOS (M1 marker); Green: CD163 (M2c marker); Blue: DAPI (nuclear staining). g Schematic of macrophage efferocytosis test toward apoptotic dHL-60 cells under different treatments. h Flow cytometry plots of dHL-60 cells before and after apoptosis induction. i Representative fluorescent images of macrophage efferocytosis toward apoptotic dHL-60 cells under different treatments. Macrophages and apoptotic cells were stained green and red, respectively. All data were generated from at least three independent experiments and presented as the means ± standard deviation. Statistical analysis was performed by one-way ANOVA. ns, not significant; ∗∗∗∗p < 0.0001.

Article Snippet: After another 48 h, macrophage cells were harvested and stained with antibodies against human iNOS (Servicebio, GB11119) and CD163 (Abcam, ab182422) for 30 min. Fluorescence images were acquired using fluorescence microscope.

Techniques: In Vitro, Migration, Comparison, Staining, Control, Fluorescence, Marker, Flow Cytometry, Generated, Standard Deviation

Journal: Bioactive Materials

Article Title: Skin-mimetic bilayer hydrogel normalizes diabetic wound healing by orchestrating inflammatory cell dynamics: An early intervention strategy

doi: 10.1016/j.bioactmat.2026.02.025

Figure Lengend Snippet: Bilayer hydrogel orchestrates inflammatory cell dynamics during the early inflammation phase of diabetic wound healing. a Experimental timeline for assay of early neutrophil recruitment. b Immunohistochemical staining for Ly-6G in wounds at 8 h, 1 d and 3 d after injury. Diabetic wounds were treated with SP/IL-10@Bilayer, SP@Bilayer, IL-10@Bilayer, and saline solution (Model), respectively. Healthy mice treated with saline solution were set as Normal. c Quantitative analysis of Ly-6G + cells in each group. d Relative expression of CXCL-1 on day 1. e Relative expression of MCP-1 on day 1. f Experimental timeline for assay of M1 macrophage infiltration. g Immunofluorescence staining for iNOS in wounds on days 1, 3 and 6 after injury. h Quantitative analysis of iNOS + cells in each group. i-k Relative expressions of macrophage-associated pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 on day 3. l Schematic illustrating the dynamic modulation of inflammatory cells during the early inflammation phase of diabetic wounds by SP/IL-10@Bilayer. All data were generated from at least three independent experiments and presented as the means ± standard deviation. Statistical analysis was performed by one-way ANOVA. # means significant difference compared to the normal group. #p < 0.05, ##p < 0.01 and ###p < 0.001; ∗ means significant difference compared to the model group. ∗p < 0.05; & means significant difference compared to SP/IL-10@Bilayer. & p < 0.05 and && p < 0.01.

Article Snippet: After another 48 h, macrophage cells were harvested and stained with antibodies against human iNOS (Servicebio, GB11119) and CD163 (Abcam, ab182422) for 30 min. Fluorescence images were acquired using fluorescence microscope.

Techniques: Immunohistochemical staining, Staining, Saline, Expressing, Immunofluorescence, Generated, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: Targeted attack: Harnessing myelin-specific plasmolipin for suppression of neuroblastoma and glioblastoma

doi: 10.1016/j.omton.2026.201154

Figure Lengend Snippet: McERV-PTLVs specifically transduce cells of brain tumors induced by GSCs injection, leaving normal brain tissues untouched (A) Mice with intracranial tumor induced by GSCs were transduced with concentrated McERV-PTLVs encoding marker EGFP. Seven days after transduction, the brain was isolated, and first cut in coronal section by the injection holes was performed. (B) Fluorescence microscopy images representing the area of the first cut demonstrate the distribution of transduced cells expressing marker EGFP. Magnified images with signed white scale bar provided. White doted lines represent the EGFP-positive area. The small image at the left upper corner of the first picture is the coronal slice stained immunohistochemically with anti-nestin antibodies representing the tumor engraftment. (C) Control group of mice was injected with 1×PBS instead of GSCs and then with McERV-PTLVs. The brain of control mice was analyzed as written above. (D) Fluorescence microscopy images of the area of the first cut represent the absence of EGFP-positive cells. The scheme of the coronal section of caudate-putamen area, where injection holes were performed (marked with red-dotted square). The small image left from the first picture is the coronal slice stained immunohistochemically with anti-nestin antibodies representing the absence of tumor. (E) Mice with intracranial tumor induced by GSCs were transduced with concentrated VSVG-PTLVs encoding marker EGFP. Black-dotted arrow below represents the timescale. (F) The fluorescence microscopy images represent the more disseminated areas of EGFP-positive cells provided on several magnifications (pointed by white arrows). The small image at the left bottom corner of the first picture is the coronal slice stained immunohistochemically, with anti-nestin antibodies representing the tumor engraftment. (G) Images of hematoxylin/eosin staining (right column) and immunohistochemical staining of slices with anti-(human) nestin antibody. Black dotted line represents the area of tumor growth. The upper row samples obtained from mice injected with GSCs and McERV-PTLVs; middle row:1×PBS and McERV-PTLVs; bottom row: GSCs and VSVG-PTLVs. Black scale bars, 100 μm. (H) Fluorescence microscopy images of IF-stained slices obtained from mice with GSC-induced tumor and injected with McERV-PTLVs. DAPI: nuclei staining (blue); anti-(human) nestin mAb stained with Alexa 555 (Red) fluor-conjugated secondary Ab, EGFP: marker fluorescent protein indicates the cells transduced with McERV-PTLVs (the merged image of EGFP [green] and anti-nestin [red] pictures are represented). The white dotted line represents the nestin-positive area of tumor growth. (I) Fluorescence microscopy images of IF-stained slices obtained from mice of control group injected with 1×PBS and McERV PTLVs, representing the absence of nestin and EGFP-positive cells. (J) Fluorescence microscopy images of IF-stained slices obtained from mice with GSC-induced tumor and injected with VSVG-PTLVs. White scale bars on H, I, and J: 100 μm.

Article Snippet: For immunohistochemical assessments, an antibody specific to human nestin (R&D Systems GmbH, Wiesbaden-Nordenstadt, Germany) was used.

Techniques: Injection, Transduction, Marker, Isolation, Fluorescence, Microscopy, Expressing, Staining, Control, Immunohistochemical staining