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eln  (Atlas Antibodies)


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    Structured Review

    Atlas Antibodies eln
    A) A fixed 5-plex panel outlines different cell types in skeletal muscle: M-I fibers (TNNC1, yellow), M-II fibers (MYH2, purple), satellite cells (PAX7, cyan), fibroblasts (FBLN2, red), and endothelial cells (CD34, white). B-C) Multiplex staining of five <t>different</t> <t>DEGs</t> is visualized in green (COL4A3, COL15A1, <t>ELN,</t> LAMB1, and XIRP2), with the top panels showing only the DEG together with DAPI, and bottom panels displaying all seven channels (5-plex panel, DEG, and DAPI). Representative images are shown for control samples, PCOS patients before treatment (PCOS week 0), and PCOS patients after 16 weeks of metformin treatment.
    Eln, supplied by Atlas Antibodies, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/eln/bio_rxiv__64898__2026__03__13__711523-370-14-16?v=Atlas+Antibodies
    Average 91 stars, based on 2 article reviews
    eln - by Bioz Stars, 2026-07
    91/100 stars

    Images

    1) Product Images from "Cell type–resolved transcriptomic map of skeletal muscle in women with polycystic ovary syndrome"

    Article Title: Cell type–resolved transcriptomic map of skeletal muscle in women with polycystic ovary syndrome

    Journal: bioRxiv

    doi: 10.64898/2026.03.13.711523

    A) A fixed 5-plex panel outlines different cell types in skeletal muscle: M-I fibers (TNNC1, yellow), M-II fibers (MYH2, purple), satellite cells (PAX7, cyan), fibroblasts (FBLN2, red), and endothelial cells (CD34, white). B-C) Multiplex staining of five different DEGs is visualized in green (COL4A3, COL15A1, ELN, LAMB1, and XIRP2), with the top panels showing only the DEG together with DAPI, and bottom panels displaying all seven channels (5-plex panel, DEG, and DAPI). Representative images are shown for control samples, PCOS patients before treatment (PCOS week 0), and PCOS patients after 16 weeks of metformin treatment.
    Figure Legend Snippet: A) A fixed 5-plex panel outlines different cell types in skeletal muscle: M-I fibers (TNNC1, yellow), M-II fibers (MYH2, purple), satellite cells (PAX7, cyan), fibroblasts (FBLN2, red), and endothelial cells (CD34, white). B-C) Multiplex staining of five different DEGs is visualized in green (COL4A3, COL15A1, ELN, LAMB1, and XIRP2), with the top panels showing only the DEG together with DAPI, and bottom panels displaying all seven channels (5-plex panel, DEG, and DAPI). Representative images are shown for control samples, PCOS patients before treatment (PCOS week 0), and PCOS patients after 16 weeks of metformin treatment.

    Techniques Used: Multiplex Assay, Staining, Control



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    Image Search Results


    Schematic Illustration of the Synergistic Therapeutic System for Diabetic Wound Repair. The schematic diagram illustrates the synergistic therapeutic mechanism of G-ELNs and SM in diabetic wound repair. G-ELNs specifically activate the MERTK receptor on macrophages, inducing their polarization toward the reparative M2c phenotype and enhancing efferocytosis to clear apoptotic cell debris and block inflammatory cascades. Meanwhile, SM hydrogel utilizes its three-dimensional porous topological structure and dynamic sustained-release properties to achieve targeted delivery and prolonged release of G-ELNs, while promoting fibroblast/endothelial cell proliferation to fuel wound regeneration. In diabetic wounds, this system exerts dual regulatory effects: phenotypically, it reshapes the anti-inflammatory microenvironment by driving macrophage M2c polarization and secretion of pro-repair factors (e.g., IL-10, TGF-β); functionally, it amplifies efferocytosis through the MERTK signaling pathway, efficiently eliminating apoptotic fragments to disrupt the “inflammation-apoptosis-necrosis” vicious cycle. This coordinated action ultimately promotes ordered collagen fiber crosslinking and vascular network maturation, accelerating tissue regeneration.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: Schematic Illustration of the Synergistic Therapeutic System for Diabetic Wound Repair. The schematic diagram illustrates the synergistic therapeutic mechanism of G-ELNs and SM in diabetic wound repair. G-ELNs specifically activate the MERTK receptor on macrophages, inducing their polarization toward the reparative M2c phenotype and enhancing efferocytosis to clear apoptotic cell debris and block inflammatory cascades. Meanwhile, SM hydrogel utilizes its three-dimensional porous topological structure and dynamic sustained-release properties to achieve targeted delivery and prolonged release of G-ELNs, while promoting fibroblast/endothelial cell proliferation to fuel wound regeneration. In diabetic wounds, this system exerts dual regulatory effects: phenotypically, it reshapes the anti-inflammatory microenvironment by driving macrophage M2c polarization and secretion of pro-repair factors (e.g., IL-10, TGF-β); functionally, it amplifies efferocytosis through the MERTK signaling pathway, efficiently eliminating apoptotic fragments to disrupt the “inflammation-apoptosis-necrosis” vicious cycle. This coordinated action ultimately promotes ordered collagen fiber crosslinking and vascular network maturation, accelerating tissue regeneration.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Blocking Assay

    Characterization and concentration screening of G-ELNs. (A) Process of exosome extraction from grapes. (B) NTA of particle size distribution for grape-derived exosomes. (C) TEM images of grape exosomes. (D) Confocal microscopy images of RAW264.7 cellular uptake of G-ELNs. (E) Proliferation of RAW264.7 cells detected via EdU labeling assay. (F) Quantitative analysis of proliferation rates. Data from 2 independent experiments (n = 2 experiments), 6 biological replicates per group, 3 technical replicates per sample. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: Characterization and concentration screening of G-ELNs. (A) Process of exosome extraction from grapes. (B) NTA of particle size distribution for grape-derived exosomes. (C) TEM images of grape exosomes. (D) Confocal microscopy images of RAW264.7 cellular uptake of G-ELNs. (E) Proliferation of RAW264.7 cells detected via EdU labeling assay. (F) Quantitative analysis of proliferation rates. Data from 2 independent experiments (n = 2 experiments), 6 biological replicates per group, 3 technical replicates per sample. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Concentration Assay, Extraction, Derivative Assay, Confocal Microscopy, Labeling

    G-ELNs promote M2 polarization of RAW264.7 macrophages in vitro. (A) Quantitative analysis of mRNA expression levels of Il-4, Il-10, Arg-1, Tgf-β , and iNOS in RAW264.7 cells across experimental groups. (B-D) Flow cytometry analysis of M1 phenotype (CD86 + ) and M2 phenotype (CD206 + ) in RAW264.7 cells treated with G-ELNs, along with quantitative assessment. (E-F) Confocal microscopy images and quantitative analysis of M2 phenotype marker CD163 + in G-ELNs-treated RAW264.7 cells. (G-H) Confocal microscopy images and quantitative analysis of M2 phenotype marker CD206 + in G-ELNs-treated RAW264.7 cells. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: G-ELNs promote M2 polarization of RAW264.7 macrophages in vitro. (A) Quantitative analysis of mRNA expression levels of Il-4, Il-10, Arg-1, Tgf-β , and iNOS in RAW264.7 cells across experimental groups. (B-D) Flow cytometry analysis of M1 phenotype (CD86 + ) and M2 phenotype (CD206 + ) in RAW264.7 cells treated with G-ELNs, along with quantitative assessment. (E-F) Confocal microscopy images and quantitative analysis of M2 phenotype marker CD163 + in G-ELNs-treated RAW264.7 cells. (G-H) Confocal microscopy images and quantitative analysis of M2 phenotype marker CD206 + in G-ELNs-treated RAW264.7 cells. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: In Vitro, Expressing, Flow Cytometry, Confocal Microscopy, Marker

    Bioinformatics analysis of G-ELNs-treated RAW264.7 cells. (A) Heatmap of differentially expressed genes (DEGs) between the Con and G-ELNs groups, with red and blue representing upregulated and downregulated expression, respectively. (B) Volcano plot of DEGs between the Con and G-ELNs groups. (C) Heatmap of the top 10 DEGs. (D) Gene Ontology (GO) biological process analysis. (E) KEGG pathway enrichment analysis. (F-H) Gene Set Enrichment Analysis (GSEA) of efferocytosis-related GO terms and KEGG pathways. (I) Molecular function enrichment map for efferocytosis-related genes, highlighting predominant enrichment in phosphatidylserine (PS) binding. (J) STRING protein-protein interaction (PPI) network for efferocytosis-related molecules, with TAM family receptors (Axl, Tyro3, MerTK) identified as classical PS receptors.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: Bioinformatics analysis of G-ELNs-treated RAW264.7 cells. (A) Heatmap of differentially expressed genes (DEGs) between the Con and G-ELNs groups, with red and blue representing upregulated and downregulated expression, respectively. (B) Volcano plot of DEGs between the Con and G-ELNs groups. (C) Heatmap of the top 10 DEGs. (D) Gene Ontology (GO) biological process analysis. (E) KEGG pathway enrichment analysis. (F-H) Gene Set Enrichment Analysis (GSEA) of efferocytosis-related GO terms and KEGG pathways. (I) Molecular function enrichment map for efferocytosis-related genes, highlighting predominant enrichment in phosphatidylserine (PS) binding. (J) STRING protein-protein interaction (PPI) network for efferocytosis-related molecules, with TAM family receptors (Axl, Tyro3, MerTK) identified as classical PS receptors.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Expressing, Binding Assay

    G-ELNs upregulate MERTK expression and enhance efferocytosis in M2c macrophages in vitro. (A) Quantitative analysis of mRNA expression levels of Mertk, Axl, Tyro3, Gas6, and Rac1 in RAW264.7 cells across experimental groups. Data parameters as A. (B, D) Flow cytometry analysis and quantitative assessment of efferocytosis in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. (C, E) Flow cytometry analysis and quantitative assessment of sustained efferocytosis (sequential apoptotic cell clearance) in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. (F, J) Confocal microscopy images and quantitative analysis of efferocytosis in G-ELNs-treated RAW264.7 cells. Data parameters as E–H. (H, I) Confocal microscopy images and quantitative analysis of MERTK protein expression in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: G-ELNs upregulate MERTK expression and enhance efferocytosis in M2c macrophages in vitro. (A) Quantitative analysis of mRNA expression levels of Mertk, Axl, Tyro3, Gas6, and Rac1 in RAW264.7 cells across experimental groups. Data parameters as A. (B, D) Flow cytometry analysis and quantitative assessment of efferocytosis in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. (C, E) Flow cytometry analysis and quantitative assessment of sustained efferocytosis (sequential apoptotic cell clearance) in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. (F, J) Confocal microscopy images and quantitative analysis of efferocytosis in G-ELNs-treated RAW264.7 cells. Data parameters as E–H. (H, I) Confocal microscopy images and quantitative analysis of MERTK protein expression in G-ELNs-treated RAW264.7 cells. Data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Expressing, In Vitro, Flow Cytometry, Confocal Microscopy

    Preparation, characterization, and cytocompatibility evaluation of SM hydrogel. (A) Schematic illustration of SM hydrogel synthesis. (B) Gelation process images. (C) SEM image. (D) Rheological profiles (storage modulus G′ and loss modulus G″) of 3%, 5%, and 10% SM hydrogels. (E) Swelling kinetics of SM hydrogels. (F) Degradation curves of SM hydrogels in PBS. (G) Cumulative release profile of G-ELNs from SM hydrogel. (H, I) Hemolysis assay images and hemolysis rate quantification for SM hydrogels at varying concentrations. (J, K) Proliferation of NIH-3T3 fibroblasts and HUVECs co-cultured with extracts from different SM hydrogel groups for 1, 3, and 5 days, measured via CCK-8 assay. (L, M) Live/dead staining images and quantification of NIH-3T3 and HUVEC cells after 3 days of incubation with SM hydrogel extracts.The above data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group, 3 technical replicates per sample. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: Preparation, characterization, and cytocompatibility evaluation of SM hydrogel. (A) Schematic illustration of SM hydrogel synthesis. (B) Gelation process images. (C) SEM image. (D) Rheological profiles (storage modulus G′ and loss modulus G″) of 3%, 5%, and 10% SM hydrogels. (E) Swelling kinetics of SM hydrogels. (F) Degradation curves of SM hydrogels in PBS. (G) Cumulative release profile of G-ELNs from SM hydrogel. (H, I) Hemolysis assay images and hemolysis rate quantification for SM hydrogels at varying concentrations. (J, K) Proliferation of NIH-3T3 fibroblasts and HUVECs co-cultured with extracts from different SM hydrogel groups for 1, 3, and 5 days, measured via CCK-8 assay. (L, M) Live/dead staining images and quantification of NIH-3T3 and HUVEC cells after 3 days of incubation with SM hydrogel extracts.The above data from 3 independent experiments (n = 3 experiments), 3 biological replicates per group, 3 technical replicates per sample. ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Hemolysis Assay, Cell Culture, CCK-8 Assay, Staining, Incubation

    In vivo evaluation of diabetic wound healing performance using SM hydrogel loaded with G-ELNs. (A) Macroscopic images of wound closure progression. (B) Wound healing trajectory mapping. (C) Quantitative analysis of wound area reduction over time. (D) Representative histopathological images of H&E, Masson's trichrome, and Sirius red staining on day 21 post-treatment. (E-G) Statistical quantification of epidermal thickness, dermal thickness, and type ⅠII/I collagen ratio. (n = 8), ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: In vivo evaluation of diabetic wound healing performance using SM hydrogel loaded with G-ELNs. (A) Macroscopic images of wound closure progression. (B) Wound healing trajectory mapping. (C) Quantitative analysis of wound area reduction over time. (D) Representative histopathological images of H&E, Masson's trichrome, and Sirius red staining on day 21 post-treatment. (E-G) Statistical quantification of epidermal thickness, dermal thickness, and type ⅠII/I collagen ratio. (n = 8), ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: In Vivo, Staining

    SM hydrogel loaded with G-ELNs promotes diabetic wound healing in rats by upregulating MERTK protein expression in M2c-subtype macrophages to enhance efferocytosis. (A) Immunofluorescence staining of CD68 and MERTK in wound tissues at days 3, 7, 14, and 21 post-treatment. (B) Quantitative analysis and statistics of CD68 + /MERTK + double-positive cells at days 7 and 14. (C-E) mRNA expression levels of Mertk, Axl, and Gas6 in skin tissues across groups at day 7. (F-H) mRNA expression levels of Mertk, Tyro3, and Axl in skin tissues across groups at day 14. (n = 8), ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: SM hydrogel loaded with G-ELNs promotes diabetic wound healing in rats by upregulating MERTK protein expression in M2c-subtype macrophages to enhance efferocytosis. (A) Immunofluorescence staining of CD68 and MERTK in wound tissues at days 3, 7, 14, and 21 post-treatment. (B) Quantitative analysis and statistics of CD68 + /MERTK + double-positive cells at days 7 and 14. (C-E) mRNA expression levels of Mertk, Axl, and Gas6 in skin tissues across groups at day 7. (F-H) mRNA expression levels of Mertk, Tyro3, and Axl in skin tissues across groups at day 14. (n = 8), ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Expressing, Immunofluorescence, Staining

    SM hydrogel loaded with G-ELNs promotes diabetic wound healing in rats by enhancing efferocytosis. (A) Immunofluorescence staining of CD68 and Caspase-3 in wound tissues at days 7 and 14 post-treatment. (B) Immunofluorescence staining of CD163 in wound tissues at days 7 and 14. (C, D) Quantitative analysis and statistical results of CD68 + /Caspase-3 + double-positive cells and CD163 + macrophages. Data parameters as B ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Activating the cellular scavenger: A bioactive hydrogel promotes diabetic wounds via plant exosome-like nanovesicles enhanced macrophage efferocytosis

    doi: 10.1016/j.bioactmat.2026.03.039

    Figure Lengend Snippet: SM hydrogel loaded with G-ELNs promotes diabetic wound healing in rats by enhancing efferocytosis. (A) Immunofluorescence staining of CD68 and Caspase-3 in wound tissues at days 7 and 14 post-treatment. (B) Immunofluorescence staining of CD163 in wound tissues at days 7 and 14. (C, D) Quantitative analysis and statistical results of CD68 + /Caspase-3 + double-positive cells and CD163 + macrophages. Data parameters as B ns:p > 0.05 ; ∗p < 0.1, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Exosome-like nanovesicles (ELNs), leveraging their natural bioactive component delivery capacity and low immunogenicity, provide a novel tool for modulating the immune microenvironment of diabetic skin ulcers.

    Techniques: Immunofluorescence, Staining

    A) A fixed 5-plex panel outlines different cell types in skeletal muscle: M-I fibers (TNNC1, yellow), M-II fibers (MYH2, purple), satellite cells (PAX7, cyan), fibroblasts (FBLN2, red), and endothelial cells (CD34, white). B-C) Multiplex staining of five different DEGs is visualized in green (COL4A3, COL15A1, ELN, LAMB1, and XIRP2), with the top panels showing only the DEG together with DAPI, and bottom panels displaying all seven channels (5-plex panel, DEG, and DAPI). Representative images are shown for control samples, PCOS patients before treatment (PCOS week 0), and PCOS patients after 16 weeks of metformin treatment.

    Journal: bioRxiv

    Article Title: Cell type–resolved transcriptomic map of skeletal muscle in women with polycystic ovary syndrome

    doi: 10.64898/2026.03.13.711523

    Figure Lengend Snippet: A) A fixed 5-plex panel outlines different cell types in skeletal muscle: M-I fibers (TNNC1, yellow), M-II fibers (MYH2, purple), satellite cells (PAX7, cyan), fibroblasts (FBLN2, red), and endothelial cells (CD34, white). B-C) Multiplex staining of five different DEGs is visualized in green (COL4A3, COL15A1, ELN, LAMB1, and XIRP2), with the top panels showing only the DEG together with DAPI, and bottom panels displaying all seven channels (5-plex panel, DEG, and DAPI). Representative images are shown for control samples, PCOS patients before treatment (PCOS week 0), and PCOS patients after 16 weeks of metformin treatment.

    Article Snippet: Primary antibodies for the DEGs were: COL4A2 (C1926, Sigma-Aldrich), COL15A1 (HPA017913, Atlas Antibodies AB), ELN (HPA018111, Atlas Antibodies AB), LAMB1 (sc-17763, Santa Cruz Biotechnology, Dallas, TX), and XIRP2 (HPA074599, Atlas Antibodies AB).

    Techniques: Multiplex Assay, Staining, Control

    PPS‐ELNs inhibited proliferation and promoted apoptosis in CRC cells. (A) The morphology and structure of PPS‐ELNs were observed by TEM. Scale bar = 100 nm. (B) The particle size and zeta potential of PPS‐ELNs were analyzed using a Malvern Zetasizer. (C) Uptake of PPS‐ELNs by HCT116 and HT‐29 cells was assessed by laser confocal microscopy. Scale bar = 25 μm. The viability of HCT116 cells (D), HT‐29 cells (E), and FHC cells (F) was measured by CCK‐8 assay. (G) The proliferation of HCT116 and HT‐29 cells was assessed by colony formation assay. (H) Apoptosis rate in HCT116 and HT‐29 cells was detected by flow cytometry. ** p < 0.01 vs. Control or 0 μg/mL group. PPS‐ELNs, Pinellia pedatisecta Schott‐derived exosome‐like nanovesicles; CRC, colorectal cancer; TEM, Transmission electron microscopy; CCK‐8, Cell counting kit‐8.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs inhibited proliferation and promoted apoptosis in CRC cells. (A) The morphology and structure of PPS‐ELNs were observed by TEM. Scale bar = 100 nm. (B) The particle size and zeta potential of PPS‐ELNs were analyzed using a Malvern Zetasizer. (C) Uptake of PPS‐ELNs by HCT116 and HT‐29 cells was assessed by laser confocal microscopy. Scale bar = 25 μm. The viability of HCT116 cells (D), HT‐29 cells (E), and FHC cells (F) was measured by CCK‐8 assay. (G) The proliferation of HCT116 and HT‐29 cells was assessed by colony formation assay. (H) Apoptosis rate in HCT116 and HT‐29 cells was detected by flow cytometry. ** p < 0.01 vs. Control or 0 μg/mL group. PPS‐ELNs, Pinellia pedatisecta Schott‐derived exosome‐like nanovesicles; CRC, colorectal cancer; TEM, Transmission electron microscopy; CCK‐8, Cell counting kit‐8.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: Zeta Potential Analyzer, Confocal Microscopy, CCK-8 Assay, Colony Assay, Flow Cytometry, Control, Derivative Assay, Transmission Assay, Electron Microscopy, Cell Counting

    PPS‐ELNs regulated the mitophagy pathway in CRC cells. The expression of p62, PINK1, Parkin, and LC3‐II/I in HCT116 cells (A) and HT‐29 cells (B) was detected by Western blot. ** p < 0.01 vs. Control group.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs regulated the mitophagy pathway in CRC cells. The expression of p62, PINK1, Parkin, and LC3‐II/I in HCT116 cells (A) and HT‐29 cells (B) was detected by Western blot. ** p < 0.01 vs. Control group.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: Expressing, Western Blot, Control

    Lysosome inhibitor suppressed mitophagy in PPS‐ELNs‐treated HCT116 cells. (A) The levels of ROS, SOD, and MDA were detected by commercial kits. (B) Autophagosomes in HCT116 cells were observed by TEM. Scale bar = 1 μm. (C) Lysosomes in HCT116 cells were detected by LysoTracker Red staining. Scale bar = 100 μm. (D) The co‐localization of LC3 and mitochondrial protein TOM20 was detected by immunofluorescence. Scale bar = 100 μm. (E) The expression of p62, PINK1, Parkin, Gal3, TOM20, and LC3‐II/I was detected by Western blot. ** p < 0.01 vs. Control group. # p < 0.05, ## p < 0.01 vs. PPS‐ELNs group. CQ, chloroquine.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: Lysosome inhibitor suppressed mitophagy in PPS‐ELNs‐treated HCT116 cells. (A) The levels of ROS, SOD, and MDA were detected by commercial kits. (B) Autophagosomes in HCT116 cells were observed by TEM. Scale bar = 1 μm. (C) Lysosomes in HCT116 cells were detected by LysoTracker Red staining. Scale bar = 100 μm. (D) The co‐localization of LC3 and mitochondrial protein TOM20 was detected by immunofluorescence. Scale bar = 100 μm. (E) The expression of p62, PINK1, Parkin, Gal3, TOM20, and LC3‐II/I was detected by Western blot. ** p < 0.01 vs. Control group. # p < 0.05, ## p < 0.01 vs. PPS‐ELNs group. CQ, chloroquine.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: Staining, Immunofluorescence, Expressing, Western Blot, Control

    PPS‐ELNs inhibited CRC progression by upregulating the lysosome‐mediated mitophagy pathway. (A) The viability of HCT116 cells was measured by CCK‐8 assay. (B) The apoptosis rate in HCT116 cells was detected by flow cytometry. (C) The expression of Bcl‐2 and Bax was detected by Western blot. ** p < 0.01 vs. Control group. ## p < 0.01 vs. PPS‐ELNs group.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs inhibited CRC progression by upregulating the lysosome‐mediated mitophagy pathway. (A) The viability of HCT116 cells was measured by CCK‐8 assay. (B) The apoptosis rate in HCT116 cells was detected by flow cytometry. (C) The expression of Bcl‐2 and Bax was detected by Western blot. ** p < 0.01 vs. Control group. ## p < 0.01 vs. PPS‐ELNs group.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: CCK-8 Assay, Flow Cytometry, Expressing, Western Blot, Control

    PPS‐ELNs inhibited tumor progression in CRC mice. (A) Representative images of the fluorescence distribution in nude mice at 6, 12, and 24 h after injection of DiR‐labeled PPS‐ELNs. (B) Representative images of in vitro fluorescence signals in major organs (heart, liver, spleen, lung, and kidney) and tumor tissues at 24 h after injection of DiR‐labeled PPS‐ELNs. (C) Tumor volume and weight of mice. (D) Apoptosis rate in tumor tissues was detected by TUNEL staining. Scale bar = 20 μm. (E) The expression of Ki67 in tumors was detected by immunohistochemistry. Scale bar = 20 μm. ** p < 0.01 vs. Control group.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs inhibited tumor progression in CRC mice. (A) Representative images of the fluorescence distribution in nude mice at 6, 12, and 24 h after injection of DiR‐labeled PPS‐ELNs. (B) Representative images of in vitro fluorescence signals in major organs (heart, liver, spleen, lung, and kidney) and tumor tissues at 24 h after injection of DiR‐labeled PPS‐ELNs. (C) Tumor volume and weight of mice. (D) Apoptosis rate in tumor tissues was detected by TUNEL staining. Scale bar = 20 μm. (E) The expression of Ki67 in tumors was detected by immunohistochemistry. Scale bar = 20 μm. ** p < 0.01 vs. Control group.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: Fluorescence, Injection, Labeling, In Vitro, TUNEL Assay, Staining, Expressing, Immunohistochemistry, Control

    PPS‐ELNs regulated lysosome‐mediated mitophagy pathway in CRC mice. (A) The expression of Gal3 in tumors was detected by immunohistochemistry. Scale bar = 20 μm. (B) Autophagosomes in tumor tissues were observed by TEM. Scale bar = 1 μm. (C) The expression of p62, TOM20, LC3‐II/I, PINK1, and Parkin was detected by Western blot. * p < 0.05, ** p < 0.01 vs. Control group.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs regulated lysosome‐mediated mitophagy pathway in CRC mice. (A) The expression of Gal3 in tumors was detected by immunohistochemistry. Scale bar = 20 μm. (B) Autophagosomes in tumor tissues were observed by TEM. Scale bar = 1 μm. (C) The expression of p62, TOM20, LC3‐II/I, PINK1, and Parkin was detected by Western blot. * p < 0.05, ** p < 0.01 vs. Control group.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: Expressing, Immunohistochemistry, Western Blot, Control

    PPS‐ELNs demonstrated favorable biocompatibility in vivo. (A) Representative images of HE staining of heart, liver, spleen, lung, and kidney tissues to assess biocompatibility. (B) Serum ALT, AST, creatinine, and UREA levels were detected by a biochemical analyzer. ALT, alanine aminotransferase; AST, aspartate aminotransferase.

    Journal: Food Science & Nutrition

    Article Title: Pinellia pedatisecta Schott‐Derived Exosome‐Like Nanovesicles Promote Apoptosis in Colorectal Cancer by Regulating the Lysosome‐Mediated Mitophagy Pathway

    doi: 10.1002/fsn3.71500

    Figure Lengend Snippet: PPS‐ELNs demonstrated favorable biocompatibility in vivo. (A) Representative images of HE staining of heart, liver, spleen, lung, and kidney tissues to assess biocompatibility. (B) Serum ALT, AST, creatinine, and UREA levels were detected by a biochemical analyzer. ALT, alanine aminotransferase; AST, aspartate aminotransferase.

    Article Snippet: Cells were simultaneously treated with 10 μg/mL PPS‐ELNs and 10 μM CQ (a lysosome inhibitor, MACKLIN, C798394) for 48 h. Subsequently, cell viability was determined by CCK‐8 assay.

    Techniques: In Vivo, Staining