Journal: Nature Communications

Article Title: Bioinspired porous metal-amino acid nanozymes enable multi-pathway treatment of atherosclerosis through anti-oxidation and pro-efferocytosis

doi: 10.1038/s41467-026-75509-4

Figure Lengend Snippet: a The synthetic process and the structure diagram of MAzyme (created in BioRender. Huang, H. (2026) https://BioRender.com/glo0g6v ). b TEM image of MAzyme and a magnification image (inset). c The high-resolution TEM image of MAzyme. d , e Elemental mapping images of MAzyme. f The structural changes of the initial and final states of the composite system in different models during the simulation process. g Temporal evolution of the self-aggregation supramolecular structure for MAzyme by MSD. h Fourier transform infrared (FTIR) spectrum of MAzyme. i High-resolution Cu 2 p X-ray photoelectron spectroscopy (XPS) results of MAzyme. j X-ray diffraction (XRD) pattern of MAzyme. k N 2 adsorption/desorption isotherms of MAzyme and the corresponding pore-size distribution curve calculated by non-local density functional theory (NLDFT, inset). l TEM image of biomimetic MMAzyme, indicating a cytomembrane layer coated on the surface of MAzyme. m Characteristic protein bands of CD36, CD47, and CCR2 on MAzyme, MMAzyme, and MM by Western blotting. n Zeta potentials and o particle diameter of MAzyme and MMAzyme analyzed by dynamic light scattering (DLS) ( n = 3 independent samples). Data in ( n , o ) were expressed as mean ± S.D. Source data are provided as a file.

Article Snippet: The following primary antibodies were used in this study: CD47 Rabbit pAb (A1838, ABclonal,1:750), CD36/SR-B3 Rabbit pAb (A5792, ABclonal,1:2500), CCR2 Rabbit pAb (A2855, ABclonal,1:750), Na-K-ATP Rabbit pAb (GB11400, Servicebio,1:2000), MERTK Rabbit pAb (A5443, ABclonal,1:750), LXRα Rabbit mAb (A3974, ABclonal,1:3000), ABCG1 Rabbit mAb (A17907, ABclonal,1:1500), PPARγ Rabbit pAb (WL01800, Wanleibio,1:1000), Anti-ABCA1 antibody ( AB307536 , Abcam,1:1000), GAPDH Rabbit pAb (AC001, ABclonal,1:20000), p-SHP1 (8849, Cell Signaling Technology, 1:1000), HRP-conjugated Goat anti-Rabbit IgG (H+L) (AS014, ABclonal,1:5000).

Techniques: Fourier Transform Infrared Spectroscopy, Spectroscopy, Adsorption, Pore Size, Functional Assay, Western Blot

Journal: Nature Communications

Article Title: Bioinspired porous metal-amino acid nanozymes enable multi-pathway treatment of atherosclerosis through anti-oxidation and pro-efferocytosis

doi: 10.1038/s41467-026-75509-4

Figure Lengend Snippet: a Schematic illustration of the pro-efferocytosis property of MMAzyme-S. (Created in BioRender. Huang, H. (2026) https://BioRender.com/7l5dwq4 ). b CLSM images depicting phagocytosis of CD47-overexpressed ACs in proinflammatory-phenotype macrophages pretreated with different samples. FCM results ( c ) and the corresponding quantitative analysis ( d ) of efferocytosis towards CD47-overexpressed ACs by proinflammatory phenotype macrophages pretreated with different samples ( n = 3 independent biological samples). e The quantitative results of the Western blotting of Mertk in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel. f Schematics illustration for the mechanism of promoting cholesterol efflux mediated by MMAzyme-S (created in BioRender. Huang, H. (2026) https://BioRender.com/o3x56t5 ). g Optical microscopy images of induced foamy cell formation in macrophages under different treatments. h Cholesterol content in the supernatant of foamy cells under different treatments ( n = 4 independent biological samples). i Western blotting analysis of Mertk, PPARγ, LXRα, ABCA1, and ABCG1 in macrophages under different treatments. Corresponding quantitative results of the Western blotting of PPARγ ( j ), LXRα ( k ), ABCA1 ( l ), and ABCG1 ( m ) in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel). Data in ( d , e , h , j – m ) were expressed as mean ± S.D. Significance in ( d , e , h , j – m ) was calculated using one-way ANOVA followed by Tukey’s post hoc test for multiple comparisons. Although the individual values of Group ii and Group iii in ( l ) do not overlap, the statistical analysis does not indicate a significant difference, possibly due to the limited sample size. Source data are provided as a file.

Article Snippet: The following primary antibodies were used in this study: CD47 Rabbit pAb (A1838, ABclonal,1:750), CD36/SR-B3 Rabbit pAb (A5792, ABclonal,1:2500), CCR2 Rabbit pAb (A2855, ABclonal,1:750), Na-K-ATP Rabbit pAb (GB11400, Servicebio,1:2000), MERTK Rabbit pAb (A5443, ABclonal,1:750), LXRα Rabbit mAb (A3974, ABclonal,1:3000), ABCG1 Rabbit mAb (A17907, ABclonal,1:1500), PPARγ Rabbit pAb (WL01800, Wanleibio,1:1000), Anti-ABCA1 antibody ( AB307536 , Abcam,1:1000), GAPDH Rabbit pAb (AC001, ABclonal,1:20000), p-SHP1 (8849, Cell Signaling Technology, 1:1000), HRP-conjugated Goat anti-Rabbit IgG (H+L) (AS014, ABclonal,1:5000).

Techniques: Western Blot, Derivative Assay, Microscopy

Journal: Advanced Science

Article Title: Genome‐Wide CRISPR Screen Identifies a microRNA Orchestrating Pleiotropic Resistance to Targeted Therapy and T Cell Immunity in Melanoma

doi: 10.1002/advs.202515158

Figure Lengend Snippet: miR‐18a regulates the TGF‐β signaling pathway to confer CD8 + T cell tolerance by targeting THBS1 . (A) Volcano plot showing differential expression of TGF‐β pathway genes, with miR‐18a‐5p targets (diamonds) and miR‐18a‐3p targets (triangles) highlighted and THBS1 labeled. (B) Western blot of THBS1 in A375‐Cas9 (control) and miR‐18a KO cells. (C) Dual‐luciferase reporter assay showing miR‐18a‐5p mimics suppress WT THBS1 3′UTR activity but not MUT 3′UTR. NC: scrambled mimic control. (D) Western blot confirming siRNA‐mediated THBS1 knockdown (438, 1955, and 2095) in miR‐18a KO A375 cells. Control: scrambled RNA. (E) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO cells co‐cultured with CD8 + T cells at various T:E ratios with scrambled RNA (NC) or si THBS1 (2095). (F) Schematic of C57BL/6 murine tumor model with miR‐18a‐5p mimic treatment. Mice were inoculated with miR‐18a KO YUMM1.7 cells and subsequently injected with 20 µL of scrambled mimic control or miR‐18a‐5p mimics. (G) Representative tumor images and tumor growth curves in miR‐18a‐5p mimic‐treated versus control mice. (H) Single‐cell UMAP of tumor tissues from control and miR‐18a‐5p mimic‐treated mice. (I) Hallmark pathway enrichment of DEGs (miR‐18a‐5p mimic versus control), showing TGF‐β suppression. FDTs: Fibroblast‐Derived Tumor cells; EDTs: Epithelial‐Derived Tumor cells. (J) Signaling interactions between FDTs and CD8 + T cells in control versus miR‐18a‐5p mimic‐treated mice. (K) Thbs1 expression across cell types in control and miR‐18a‐5p mimic‐treated mice. (L) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO A375 cells with/without CD8 + T cell and CD47 inhibitor (magrolimab; isotype IgG control). (M, N) Representative IHC images (M) and quantification (N) of Ki67, Cd47, and Thbs1 in murine tumor tissues. Data represent means ± SD; n = 3 biologically independent samples for panels C and E, n = 6 for panel L, and n = 7 for panels G and N. Two‐way ANOVA followed by Tukey's post hoc test is used to calculate P ‐values in panel G and unpaired two‐tailed Student's t ‐test is used to calculate P ‐values in panels C, E, L, and N: *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant.

Article Snippet: Primary antibodies used were as follows: phospho‐MEK (Cell Signaling Technology, 3958S, RRID: AB_2138014; 1:1,000), total MEK (Cell Signaling Technology, 4694S, RRID: AB_10695868; 1:2,000), phospho‐AKT (Cell Signaling Technology, 4060S, RRID: AB_2315049; 1:1,000), total AKT (Cell Signaling Technology, 2920S, RRID: AB_1147620; 1:2,000), phospho‐ERK (Cell Signaling Technology, 4377S, RRID: AB_331775; 1:1,000), total ERK (Cell Signaling Technology, 4695S, RRID: AB_390779; 1:2,000), AJUBA (ABclonal, A22039, RRID: AB_3719524; 1:2,000), CD47 (ABclonal, A11382, RRID: AB_2861554; 1:2,000), THBS1 (ABclonal, A2125, RRID: AB_2764144; 1:2,000), and hnRNP A1 (ABclonal, A11564, RRID: AB_2861599; 1:2,000). β‐actin (ABclonal, AC026, RRID: AB_2768234; 1:10,000) or GAPDH (ABclonal, AC001, RRID: AB_2619673; 1:10,000) served as loading controls.

Techniques: Quantitative Proteomics, Labeling, Western Blot, Control, Luciferase, Reporter Assay, Activity Assay, Knockdown, Cell Culture, Injection, Single Cell, Derivative Assay, Expressing, Two Tailed Test

Journal: Aging Cell

Article Title: Galectin‐9 high Neutrophils Exacerbate Radiation‐Induced Frailty

doi: 10.1111/acel.70448

Figure Lengend Snippet: GAL‐9 protein is an important regulatory molecule in neutrophil hyperactivity. (A) Intracellular GAL‐9 protein expression of circulating neutrophils in the sham group and 80 days post‐radiation. n = 6. (B) Circulating GAL‐9 protein level by ELISA kits. n = 8. (C, D) (C) Scheme and (D) the IFN‐γ expression of circulating neutrophils in the sham group under different conditions. n = 3. (E–M) (E) Scheme of the IFN‐γ and NETs expression of circulating neutrophils in the sham group by treatment with (F, H, K) circulating serum at 80 days post‐radiation and (F, I, L) culture supernatant of GAL‐9 high neutrophils. (F, J, M) IFN‐γ and NETs expression of GAL‐9 high neutrophils 80 days post‐radiation under different stimuli. n = 4–5. (N–Q) Assessment of the effect of GAL‐9 protein on the polarization of bone marrow macrophages under different conditions. (N) The scheme and the effect of (O) rmGAL‐9 protein, (P) culture supernatant of GAL‐9 high neutrophils, and (Q) circulating serum at 80 days post‐radiation were shown. n = 3. (R–S) Representative plots and statistics of bone marrow CD47 + neutrophils in the sham group and 80 days post‐radiation. n = 4. (T‐BB) Assessment of the reversal effect of GAL‐9 intervention in mice. (T) Scheme of the administration of anti‐GAL‐9 and rmGAL‐9 proteins in the local radiation group and the sham group, respectively. (U) Circulating GAL‐9 high neutrophils, bone marrow (V) CMP cells, (W) CLP cells, (X) non‐immune cells, (Y) macrophages, and (Z, AA) their polarization state and (BB) frailty index score were shown after different treatments in the local radiation group and the sham group. n = 3–5. Data are presented as mean ± SD; each dot represents an individual animal from at least 2–4 independent experiments that used male and female mice. ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001. Statistical analyses were performed using unpaired Student's t ‐test (A, B, S, U), one‐way ANOVA (D, G–M, V–AA), and two‐way ANOVA (O–Q).

Article Snippet: Primary antibodies used were Gal‐9 (1:500, Abcam #ab69630), Myeloperoxidase (1:50, Abcam #ab90810), Histone H3 (1:1000, Abcam #ab281584), Ly6g + Ly6c (1:500, Abcam #ab25377), and CD47 (1:500, Abmart #T55251S).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay