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mouse monocyte macrophages  (ATCC)


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    Structured Review

    ATCC mouse monocyte macrophages
    Schematic illustration of the preparation of CPs@SS31, and the corresponding in vivo therapy of acute lung injury via NIR enhanced ROS scavenging, inflammation inhibition, <t>macrophage</t> M2 polarization, and T cells immunoactivation, as well as specifically targeting mitochondria, activating mitochondrial function, and inducing mitophagy to reprogram lung redox homeostasis, and promote tissue repair.
    Mouse Monocyte Macrophages, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 24224 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+macrophages/RAW+264%2E7/pmc12969342-83-4-8
    Average 99 stars, based on 24224 article reviews
    mouse monocyte macrophages - by Bioz Stars, 2026-09
    99/100 stars

    Images

    1) Product Images from "Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy"

    Article Title: Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.02.040

    Schematic illustration of the preparation of CPs@SS31, and the corresponding in vivo therapy of acute lung injury via NIR enhanced ROS scavenging, inflammation inhibition, macrophage M2 polarization, and T cells immunoactivation, as well as specifically targeting mitochondria, activating mitochondrial function, and inducing mitophagy to reprogram lung redox homeostasis, and promote tissue repair.
    Figure Legend Snippet: Schematic illustration of the preparation of CPs@SS31, and the corresponding in vivo therapy of acute lung injury via NIR enhanced ROS scavenging, inflammation inhibition, macrophage M2 polarization, and T cells immunoactivation, as well as specifically targeting mitochondria, activating mitochondrial function, and inducing mitophagy to reprogram lung redox homeostasis, and promote tissue repair.

    Techniques Used: In Vivo, Inhibition

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    Activity Assay:

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    Cell Culture:

    Article Title: Injectable Particulated Human Acellular Dermal Matrix Booster for Skin Restoration: An Integrated Randomized, Split-Face, Double-Blinded Clinical Trial and Preclinical Study.
    Article Snippet: .. Cell Culture HDFs (Thermo Fisher Scientific, Waltham, MA, USA), used for the evaluation of anti-wrinkle efficacy; mouse melanoma cells (B16F10, American Type Culture Collection, Manassas, VA, USA), used for the evaluation of skin-whitening efficacy; and mouse macrophages (RAW 264.7, American Type Culture Collection), used for the evaluation of https://doi.org/10.3390/ijms27052193 anti-inflammatory efficacy, were cultured in Dulbecco’s Modified Eagle Medium (DMEM; Lonza, Walkersville, MD, USA) supplemented with 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA) and 1% penicillin–streptomycin (Gibco). .. HEKs (Thermo Fisher Scientific), used for the evaluation of moisturizing efficacy, were cultured in EpiLifeTM Medium (Gibco) supplemented with Human Keratinocyte Growth Supplement (Gibco).

    Article Title: Injectable Particulated Human Acellular Dermal Matrix Booster for Skin Restoration: An Integrated Randomized, Split-Face, Double-Blinded Clinical Trial and Preclinical Study
    Article Snippet: .. HDFs (Thermo Fisher Scientific, Waltham, MA, USA), used for the evaluation of anti-wrinkle efficacy; mouse melanoma cells (B16F10, American Type Culture Collection, Manassas, VA, USA), used for the evaluation of skin-whitening efficacy; and mouse macrophages (RAW 264.7, American Type Culture Collection), used for the evaluation of anti-inflammatory efficacy, were cultured in Dulbecco’s Modified Eagle Medium (DMEM; Lonza, Walkersville, MD, USA) supplemented with 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA) and 1% penicillin–streptomycin (Gibco). .. HEKs (Thermo Fisher Scientific), used for the evaluation of moisturizing efficacy, were cultured in EpiLifeTM Medium (Gibco) supplemented with Human Keratinocyte Growth Supplement (Gibco).

    Article Title: Antithrombotic and antibacterial surface coating based on spiky silver nanoparticles: A counterattack against clotting and biofilm
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    Article Title: Nanocomposite scaffolds incorporating ginsenoside Rg1-loaded ZIF-8 nanoparticles for enhanced osteogenesis and bone regeneration
    Article Snippet: .. Mouse macrophages (J774A.1 cell line, ATCC) were then seeded onto the nanocomposite scaffolds at a density of 40,000 cells per cm2 and cultured for 48 h. The cells were then treated with 1 μg/mL ultrapure LPS (Sigma Aldrich, USA) for 12 h. The levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1) released by the cells were measured using ELISA kits (Abcam, USA). ..

    Modification:

    Article Title: Injectable Particulated Human Acellular Dermal Matrix Booster for Skin Restoration: An Integrated Randomized, Split-Face, Double-Blinded Clinical Trial and Preclinical Study.
    Article Snippet: .. Cell Culture HDFs (Thermo Fisher Scientific, Waltham, MA, USA), used for the evaluation of anti-wrinkle efficacy; mouse melanoma cells (B16F10, American Type Culture Collection, Manassas, VA, USA), used for the evaluation of skin-whitening efficacy; and mouse macrophages (RAW 264.7, American Type Culture Collection), used for the evaluation of https://doi.org/10.3390/ijms27052193 anti-inflammatory efficacy, were cultured in Dulbecco’s Modified Eagle Medium (DMEM; Lonza, Walkersville, MD, USA) supplemented with 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA) and 1% penicillin–streptomycin (Gibco). .. HEKs (Thermo Fisher Scientific), used for the evaluation of moisturizing efficacy, were cultured in EpiLifeTM Medium (Gibco) supplemented with Human Keratinocyte Growth Supplement (Gibco).

    Article Title: Injectable Particulated Human Acellular Dermal Matrix Booster for Skin Restoration: An Integrated Randomized, Split-Face, Double-Blinded Clinical Trial and Preclinical Study
    Article Snippet: .. HDFs (Thermo Fisher Scientific, Waltham, MA, USA), used for the evaluation of anti-wrinkle efficacy; mouse melanoma cells (B16F10, American Type Culture Collection, Manassas, VA, USA), used for the evaluation of skin-whitening efficacy; and mouse macrophages (RAW 264.7, American Type Culture Collection), used for the evaluation of anti-inflammatory efficacy, were cultured in Dulbecco’s Modified Eagle Medium (DMEM; Lonza, Walkersville, MD, USA) supplemented with 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA) and 1% penicillin–streptomycin (Gibco). .. HEKs (Thermo Fisher Scientific), used for the evaluation of moisturizing efficacy, were cultured in EpiLifeTM Medium (Gibco) supplemented with Human Keratinocyte Growth Supplement (Gibco).

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    Article Snippet: .. Mouse endothelial cells (SVEC4-10, ATCC CRL-2181, passages 10) and mouse macrophages (RAW 264.7, ATCC TIB-71, passage 20) were cultured in low-glucose Dulbecco's Modified Eagle's Medium (DMEM, Thermo Fisher Scientific Inc., Massachusetts, USA) supplemented with 10 % fetal bovine serum and 1 % penicillin/streptomycin. ..

    Enzyme-linked Immunosorbent Assay:

    Article Title: Nanocomposite scaffolds incorporating ginsenoside Rg1-loaded ZIF-8 nanoparticles for enhanced osteogenesis and bone regeneration
    Article Snippet: .. Mouse macrophages (J774A.1 cell line, ATCC) were then seeded onto the nanocomposite scaffolds at a density of 40,000 cells per cm2 and cultured for 48 h. The cells were then treated with 1 μg/mL ultrapure LPS (Sigma Aldrich, USA) for 12 h. The levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1) released by the cells were measured using ELISA kits (Abcam, USA). ..



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    Image Search Results


    Schematic illustration of the preparation of CPs@SS31, and the corresponding in vivo therapy of acute lung injury via NIR enhanced ROS scavenging, inflammation inhibition, macrophage M2 polarization, and T cells immunoactivation, as well as specifically targeting mitochondria, activating mitochondrial function, and inducing mitophagy to reprogram lung redox homeostasis, and promote tissue repair.

    Journal: Bioactive Materials

    Article Title: Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy

    doi: 10.1016/j.bioactmat.2026.02.040

    Figure Lengend Snippet: Schematic illustration of the preparation of CPs@SS31, and the corresponding in vivo therapy of acute lung injury via NIR enhanced ROS scavenging, inflammation inhibition, macrophage M2 polarization, and T cells immunoactivation, as well as specifically targeting mitochondria, activating mitochondrial function, and inducing mitophagy to reprogram lung redox homeostasis, and promote tissue repair.

    Article Snippet: Cell viability testing : Mouse monocyte macrophages (RAW264.7, ATCC, USA) were cultured in DMEM containing 10% FBS and 1% penicillin-streptomycin (Solarbio, China).

    Techniques: In Vivo, Inhibition

    Apoe deficiency increases neutral lipid accumulation in lipid-loaded BMDMs (A) Schematic overview of BMDM isolation and BODIPY 493/503 staining. Bone marrow cells were isolated from WT and Apoe −/− mice and differentiated into BMDMs with M-CSF for 7 days. (B–D) Representative flow cytometry histograms and quantification of BODIPY 493/503 signal in WT and Apoe −/− BMDMs under untreated conditions (B) , after OA treatment (200 μM, 24 h) (C) , and after oxLDL treatment (50 μg/mL, 24 h) (D) . BODIPY 493/503 fluorescence was quantified as background-subtracted median fluorescence intensity (ΔMedian MFI). Data are shown as mean ± SEM. n = 3 biological replicates per group. P values were calculated using unpaired two-tailed Welch’s t-tests. ns, not significant; ** P < 0.01 ; *** P < 0.001 . OA, oleic acid; oxLDL, oxidized low-density lipoprotein; M-CSF, macrophage colony-stimulating factor; BMDMs, bone marrow-derived macrophages.

    Journal: Frontiers in Immunology

    Article Title: APOE -associated lipid-handling macrophages in hepatocellular carcinoma: ligand–receptor communication and host Apoe -linked myeloid remodeling

    doi: 10.3389/fimmu.2026.1902143

    Figure Lengend Snippet: Apoe deficiency increases neutral lipid accumulation in lipid-loaded BMDMs (A) Schematic overview of BMDM isolation and BODIPY 493/503 staining. Bone marrow cells were isolated from WT and Apoe −/− mice and differentiated into BMDMs with M-CSF for 7 days. (B–D) Representative flow cytometry histograms and quantification of BODIPY 493/503 signal in WT and Apoe −/− BMDMs under untreated conditions (B) , after OA treatment (200 μM, 24 h) (C) , and after oxLDL treatment (50 μg/mL, 24 h) (D) . BODIPY 493/503 fluorescence was quantified as background-subtracted median fluorescence intensity (ΔMedian MFI). Data are shown as mean ± SEM. n = 3 biological replicates per group. P values were calculated using unpaired two-tailed Welch’s t-tests. ns, not significant; ** P < 0.01 ; *** P < 0.001 . OA, oleic acid; oxLDL, oxidized low-density lipoprotein; M-CSF, macrophage colony-stimulating factor; BMDMs, bone marrow-derived macrophages.

    Article Snippet: Bone marrow cells from WT and Apoe −/− mice were differentiated into bone marrow-derived macrophages (BMDMs) with macrophage colony-stimulating factor (M-CSF; 25 ng/mL; MedChemExpress, HY-P7085) for 7 days.

    Techniques: Isolation, Staining, Flow Cytometry, Fluorescence, Two Tailed Test, Derivative Assay

    In vitro evaluation of foam cell lipid accumulation and lipophagy activation following OPN-HMCN@MLT treatment. ( A - C ) ORO and BODIPY staining images and corresponding quantification of ORO and BODIPY positive areas of RAW264.7 cells under different stimulations (n = 5, scale bar for ORO: 100 μm, scale bar for BODIPY: 20 μm). ( D ) Bio-TEM images of RAW264.7 cells post various treatments (n = 5, scale bars 1.0 μm). Green arrows indicate nanoparticles. ( E , F ) Morphometric analysis determined the mean number and area (μm 2 ) of LDs per cell section. ( G ) Confocal images depicting lipophagy flux in foam cells following different treatments (n = 5 biological replicates, scale bars: 10 μm). ( H - J ) The quantities of acidified autophagosomes (GFP-RFP+), neutral autophagosomes (GFP + RFP+), and LDs labeled with BODIPY were measured per cell for each condition. (K to N) Representative Western blot images and quantitative analysis of LC3, LAMP1, and P62 expression in foam cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: In vitro evaluation of foam cell lipid accumulation and lipophagy activation following OPN-HMCN@MLT treatment. ( A - C ) ORO and BODIPY staining images and corresponding quantification of ORO and BODIPY positive areas of RAW264.7 cells under different stimulations (n = 5, scale bar for ORO: 100 μm, scale bar for BODIPY: 20 μm). ( D ) Bio-TEM images of RAW264.7 cells post various treatments (n = 5, scale bars 1.0 μm). Green arrows indicate nanoparticles. ( E , F ) Morphometric analysis determined the mean number and area (μm 2 ) of LDs per cell section. ( G ) Confocal images depicting lipophagy flux in foam cells following different treatments (n = 5 biological replicates, scale bars: 10 μm). ( H - J ) The quantities of acidified autophagosomes (GFP-RFP+), neutral autophagosomes (GFP + RFP+), and LDs labeled with BODIPY were measured per cell for each condition. (K to N) Representative Western blot images and quantitative analysis of LC3, LAMP1, and P62 expression in foam cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Article Snippet: RAW264.7 mouse macrophage cells (ATCC® TIB-71; RRID: CVCL_0493) and MCAECs (Procell, CP-M081) were cultured in Dulbecco's Modified Eagle Medium (DMEM) with 10% fetal bovine serum and 1% penicillin-streptomycin at 37 °C in a 5% CO 2 atmosphere.

    Techniques: In Vitro, Activation Assay, Staining, Labeling, Western Blot, Expressing

    In vitro examination of LD degradation in foam cells through fatty acid oxidation and cholesterol efflux. (A ) Schematic diagram of the LD degradation mechanism. ( B , C ) Confocal images and quantitative analysis of LDs colocalization with fatty acids in RAW264.7 cells following different treatments (n = 5, scale bars: 5 μm). ( D , E ) Confocal images of the colocalization of mitochondria with fatty acids and quantified data of fatty acids in RAW264.7 cells under different stimulations (n = 5, scale bars: 5 μm). ( F , G ) Confocal images illustrating mitochondrial colocalization with ATP and corresponding quantification of ATP levels in RAW264.7 cells post various treatments (n = 5, scale bars: 20 μm). ( H ) Diagram illustrating the incorporation of [U- 13 C] palmitic acid into the TCA cycle and the labeling pattern of derived metabolites (n = 3). ( I ) A PCA plot illustrates the cluster separation between the two groups (n = 3). ( J ) Heatmap showing differences in metabolites between the two groups (n = 3). ( K ) Normalized total labeling of each metabolite to [U- 13 C] palmitic acid (n = 3). ( L ) Proportion of (m + 2)-labeled TCA cycle metabolites derived from [U- 13 C] palmitic acid (n = 3). ( M - R ) The study quantified NBD-cholesterol accumulation ( M , P ) and cholesterol efflux facilitated by HDL ( N , O ) and apoA-I ( Q , R ) using confocal imaging across (n = 5, Scale bar = 50 μm). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: In vitro examination of LD degradation in foam cells through fatty acid oxidation and cholesterol efflux. (A ) Schematic diagram of the LD degradation mechanism. ( B , C ) Confocal images and quantitative analysis of LDs colocalization with fatty acids in RAW264.7 cells following different treatments (n = 5, scale bars: 5 μm). ( D , E ) Confocal images of the colocalization of mitochondria with fatty acids and quantified data of fatty acids in RAW264.7 cells under different stimulations (n = 5, scale bars: 5 μm). ( F , G ) Confocal images illustrating mitochondrial colocalization with ATP and corresponding quantification of ATP levels in RAW264.7 cells post various treatments (n = 5, scale bars: 20 μm). ( H ) Diagram illustrating the incorporation of [U- 13 C] palmitic acid into the TCA cycle and the labeling pattern of derived metabolites (n = 3). ( I ) A PCA plot illustrates the cluster separation between the two groups (n = 3). ( J ) Heatmap showing differences in metabolites between the two groups (n = 3). ( K ) Normalized total labeling of each metabolite to [U- 13 C] palmitic acid (n = 3). ( L ) Proportion of (m + 2)-labeled TCA cycle metabolites derived from [U- 13 C] palmitic acid (n = 3). ( M - R ) The study quantified NBD-cholesterol accumulation ( M , P ) and cholesterol efflux facilitated by HDL ( N , O ) and apoA-I ( Q , R ) using confocal imaging across (n = 5, Scale bar = 50 μm). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Article Snippet: RAW264.7 mouse macrophage cells (ATCC® TIB-71; RRID: CVCL_0493) and MCAECs (Procell, CP-M081) were cultured in Dulbecco's Modified Eagle Medium (DMEM) with 10% fetal bovine serum and 1% penicillin-streptomycin at 37 °C in a 5% CO 2 atmosphere.

    Techniques: In Vitro, Labeling, Derivative Assay, Imaging

    In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of HMCN@Cy5.5 , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: In vivo photoacoustic imaging and analysis of the vulnerability of atherosclerotic plaque. ( A - G ) Ex vivo distribution of HMCN@Cy5.5 , Scr-HMCN@Cy5.5 , and OPN-HMCN@Cy5.5 in various organs—specifically the aorta ( B ), heart ( C ), liver ( D ), spleen ( E ), lung ( F ), and kidney ( G )—from apoE −/− mice at 0, 6, 12, and 24 h post-intravenous injection (n = 3). ( H ) Confocal images demonstrate the colocalization of OPN with CY5.5-labeled nanoparticles in aortic roots (n = 6, scale bars, 200 μm). ( I ) Quantitative analysis of the relative MFI of OPN and CY5.5 in different treatment groups. ( J , K ) Photoacoustic images and quantitative analysis of signal intensities of atherosclerotic plaque in carotid arteries of both healthy and atherosclerosis mice (n = 3). For each animal, longitudinal PA imaging was performed on the same carotid artery at predefined anatomical landmarks across different time points. Photoacoustic images were acquired with depth calibration based on acoustic time-of-flight measurements, converting ultrasound echo delay into depth using the predefined sound velocity in soft tissue. A calibrated depth scale bar is shown in each image, with an effective imaging depth of approximately 7 mm. ( L , M ) Pathological staining of atherosclerotic plaques in the carotid artery and aortic arch includes ORO and Masson staining (scale bar = 200 μm), as well as α -SMA, and CD68 fluorescent staining (scale bar = 100 μm each). ( N - Q ) The statistical analysis of ( N ) ORO staining (namely the percentage of LD area), ( O ) Masson staining (namely the percentage of collagen fiber area), ( P ) α -SMA fluorescent staining (namely the percentage of smooth muscle cell area) and ( Q ) CD68 fluorescent staining (namely the percentage of macrophage-derived foam cell area). ( R ) Vulnerability scores of aortic arch and carotid artery plaques. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗∗ P < 0.0001.

    Article Snippet: Mouse macrophage cell line (RAW264.7) was obtained from the American Type Culture Collection, USA.

    Techniques: In Vivo, Imaging, Ex Vivo, Injection, Labeling, Staining, Derivative Assay

    In vivo atherosclerosis reversal. ( A ) Schematic illustration of the experimental timeline and treatment strategy for establishing a mature, vulnerable atherosclerosis model and evaluating therapeutic interventions. Mice were fed a high-fat diet (HFD) for 12 weeks and then divided into five groups (HFD+ 12W, Saline HFD+, OPN-HMCN@MLT HFD+, Saline HFD−, and OPN-HMCN@MLT HFD−). Except for the HFD+ 12W group, the remaining groups were further maintained for an additional 4 weeks under either HFD or non-HFD conditions with the indicated treatments. ( B , C ) Images of en face ORO-stained aortas ( B ) and quantitative analysis of ORO-positive regions ( C ) from mice subjected to different treatments and diets (n = 6, scale bar: 5 mm). ( D ) Aortic root sections stained by ORO, H&E, α-SMA antibody, Masson's trichrome, CD68 antibody, and MMP-9 antibody, respectively, following various therapeutic procedures (n = 6, scale bar: 500 μm). ( E - J ) Quantitative data of lipid accumulation ( E ), necrotic core area ( F ), collagen area ( G ), MMP-9 level ( H ), VSMC area ( I ), and macrophage-foam cell area ( J ) in aortic root sections. ( K ) Vulnerability scores of aortic root plaque. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: In vivo atherosclerosis reversal. ( A ) Schematic illustration of the experimental timeline and treatment strategy for establishing a mature, vulnerable atherosclerosis model and evaluating therapeutic interventions. Mice were fed a high-fat diet (HFD) for 12 weeks and then divided into five groups (HFD+ 12W, Saline HFD+, OPN-HMCN@MLT HFD+, Saline HFD−, and OPN-HMCN@MLT HFD−). Except for the HFD+ 12W group, the remaining groups were further maintained for an additional 4 weeks under either HFD or non-HFD conditions with the indicated treatments. ( B , C ) Images of en face ORO-stained aortas ( B ) and quantitative analysis of ORO-positive regions ( C ) from mice subjected to different treatments and diets (n = 6, scale bar: 5 mm). ( D ) Aortic root sections stained by ORO, H&E, α-SMA antibody, Masson's trichrome, CD68 antibody, and MMP-9 antibody, respectively, following various therapeutic procedures (n = 6, scale bar: 500 μm). ( E - J ) Quantitative data of lipid accumulation ( E ), necrotic core area ( F ), collagen area ( G ), MMP-9 level ( H ), VSMC area ( I ), and macrophage-foam cell area ( J ) in aortic root sections. ( K ) Vulnerability scores of aortic root plaque. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Article Snippet: Mouse macrophage cell line (RAW264.7) was obtained from the American Type Culture Collection, USA.

    Techniques: In Vivo, Saline, Staining

    In vivo anti-atherosclerosis effects. ( A ) Diagram illustrating the treatment protocol for apoE −/− mice. ( B , C ) En face ORO staining images and quantitative analysis of the lesion area of aortic lesion areas in apoE −/− mice following various treatments (n = 6, scale bar: 5 mm). ( D ) Quantification of the reduction ratio (versus model) of ORO-positive area to the entire aorta. ( E ) Cross-sectional images of ORO-stained aortic root (scale bars, 500 μm) and brachiocephalic artery (scale bars, 200 μm). n = 6. ( F and G ) Quantitative analysis of the aortic root lesion area ( F ) and the reduction ratio (versus model) of ORO-positive area to the aortic root ( G ). ( H ) Aortic root sections stained by H&E, α-SMA antibody, Masson's trichrome, CD68 antibody, MMP-9 antibody, and OPN antibody, respectively, following various therapeutic procedures (n = 6, scale bar: 500 μm). ( I-M ) Quantitative data of necrotic core area ( I ), collagen area ( J ), VSMC area ( K ), macrophage-foam cell area ( L ), and MMP-9 level ( M ) in aortic root sections. ( N ) Representative TEM images of LDs in the aortic root and arch of apoE −/− mice following various treatments (scale bar: 1 μm). The green arrow indicates elastic fibers. ( O-R ) Quantification of lipid droplet number and average area per cell section, n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: In vivo anti-atherosclerosis effects. ( A ) Diagram illustrating the treatment protocol for apoE −/− mice. ( B , C ) En face ORO staining images and quantitative analysis of the lesion area of aortic lesion areas in apoE −/− mice following various treatments (n = 6, scale bar: 5 mm). ( D ) Quantification of the reduction ratio (versus model) of ORO-positive area to the entire aorta. ( E ) Cross-sectional images of ORO-stained aortic root (scale bars, 500 μm) and brachiocephalic artery (scale bars, 200 μm). n = 6. ( F and G ) Quantitative analysis of the aortic root lesion area ( F ) and the reduction ratio (versus model) of ORO-positive area to the aortic root ( G ). ( H ) Aortic root sections stained by H&E, α-SMA antibody, Masson's trichrome, CD68 antibody, MMP-9 antibody, and OPN antibody, respectively, following various therapeutic procedures (n = 6, scale bar: 500 μm). ( I-M ) Quantitative data of necrotic core area ( I ), collagen area ( J ), VSMC area ( K ), macrophage-foam cell area ( L ), and MMP-9 level ( M ) in aortic root sections. ( N ) Representative TEM images of LDs in the aortic root and arch of apoE −/− mice following various treatments (scale bar: 1 μm). The green arrow indicates elastic fibers. ( O-R ) Quantification of lipid droplet number and average area per cell section, n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Article Snippet: Mouse macrophage cell line (RAW264.7) was obtained from the American Type Culture Collection, USA.

    Techniques: In Vivo, Staining

    Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

    Journal: Bioactive Materials

    Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

    doi: 10.1016/j.bioactmat.2026.02.041

    Figure Lengend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

    Article Snippet: Mouse macrophage cell line (RAW264.7) was obtained from the American Type Culture Collection, USA.

    Techniques: Binding Assay, Construct, Expressing