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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Murray’s law is derived from assuming minimal work in maintaining blood transport, leading to vessel radii scaling with the cube root of flow rate.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Murray’s law also assumes, constant uniform metabolic demand of the tissue, laminar flow and that blood is a Newtonian fluid.
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PMC12408821
|
Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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In contrast, the West, Brown, and Enquist (WBE) model describes vascular networks as fractal-like structures that optimise metabolic energy distribution across the vascular network in its entirety.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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It predicts a 0.5 scaling exponent for large vessels and 0.33 for small vessels, accounting for hierarchical branching, where the emphasis is on efficiently delivering nutrients and waste exchange throughout the system.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Both models provide insights into vascular architecture but differ in scope, with real vascular networks often deviating due to biological variability and tissue-specific adaptations.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Calculation of the radial exponent is done in this work following the regression-based method outlined in refs. .
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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For each vessel in the network, the number of downstream endpoints of the network is counted.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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The radius and number of downstream tips are related by Eq 4.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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from ref. :
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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3[12pt] $$ \,_^$$αNdaWhere = radius of a vessel in the network, = the number of downstream endpoints from that vessel, =the radial scaling exponent.
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PMC12408821
|
Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Plotting the log-log relation of these two variables allows a to be estimated by regression analysis.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Segmentation of the compartments within the human kidney, including cortex, medulla, intermedullary pillars and hilum, was performed in Dragonfly (version: 2021.3) using a 2D convolutional neural network (CNN).
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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The final hyperparameters of the CNN are given in Supplementary Table 4.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Correction of the CNN output was manually performed in by an expert in Amira-Avizo v2021.1 to provide the final compartment delineations.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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These compartments were used to group and then analyse vascular network parameters.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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40 3D patches (512 × 512 × 512) of the highest resolution data, captured at 2.6–5.6 µm per voxel, were extracted from multiple human kidneys scanned by HiP-CT, and the glomeruli were manually segmented.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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The widely utilised network nnU-net was trained using 35:5 cubes for a train:test split and a 70:30 training validation split.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Training using 5-fold cross validation achieved a final DICE score of 0.928, 0.860, 0.906 for training, validation and test data, respectively.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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See Supplementary Note 3 for training results and nnU-net configuration.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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The plan files detailing all parameters for the training nnU-net are provided in Supplementary data.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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This trained network was used to perform inference of two VOIs of high-resolution data from the human kidney in this study, and count the number of glomeruli in each.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Utilising the kidney anatomical compartment segmentation from above, the volume of cortical tissue within these high-resolution VOIs was calculated.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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For each VOI, the number of glomeruli and the volume of cortex in each VOI were used to estimate the total number of glomeruli in the entire kidney.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Estimates of total glomerular number extrapolated to the entire kidney, from each VOI, were: 1.28 × 10 and 1.12 × 10 for VOI 3.1 and VOI 2.1, respectively.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Statistical comparisons of vascular network morphology between human and rat kidney were performed in GraphPad Prism (version: 10.1.2).
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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For all statistical tests, a p-value of less than 0.05 was considered statistically significant.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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In both the rat and human datasets, the segmental/feeding renal arteries were identified to be at Strahler orders 8 and truncated Strahler order 9, respectively.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Radius against Strahler order were normalised to the 9th truncated Strahler order of the human data.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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Log of radius against truncated Strahler generation for the human kidney; and radius against Strahler Order of the rat kidney, were plotted facilitating a linear least squares regression analysis.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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A sum of squares F test was performed with the null hypothesis that a single set of global parameters for slope and intercept would fit vessel radius or vessel length for both the rat and human cases.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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For calculating the fit of the radial scaling exponent (a), we followed the approach of ref.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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applying a Standard major axis regression to account for measurement error in both variables.
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PMC12408821
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Mapping the arterial vascular network in an intact human kidney using hierarchical phase-contrast tomography.
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This was performed in Matlab 2023a using the gmregress.m function with an alpha significance set to 0.05.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Triple‐negative breast cancer (TNBC), a leading cause of female mortality worldwide, presents a treatment challenge due to the lack of targeted receptors.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Macrophages, recognized for their role in the immune response, provide a promising avenue for cancer research.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Given that macrophages secrete extracellular particles (EPs), which have been implicated in biological processes, including intercellular communication and immune modulation, it is hypothesized that EPs derived from macrophages could have potential anticancer effects.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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This study examines the effect of M1 macrophage‐secreted EPs on TNBC cells to investigate their potential as a therapeutic.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Polarization was induced in RAW 264.7 macrophages and characterized using ELISA, nitrite release, and microscopy.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Macrophage‐derived EPs were isolated and characterized using nanoparticle tracking analysis, electron microscopy, and western blotting.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The influence of EPs on MDA‐MB‐231 cells, a TNBC model, was assessed using confocal microscopy.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Results showed the increasing expression of caspase 3/7 in a time‐dependent manner (0, 24, and 48 h).
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Cell death was observed in TNBC cells with M1 macrophage‐derived EPs, while cell proliferation was observed when M2 macrophage‐derived EPs interacted with MDA‐MB‐231 cells.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Overall, results showed that EPs derived from M1 macrophages could induce cell death in MDA‐MB‐321 cells, opening up potential options for new treatments in TNBC.Breast cancer is the leading cause of death in women worldwide [1, 2].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Among the different types of breast cancer, they are named according to their respective receptor presence, namely human epidermal growth factor receptor (HER) 2 positive, progesterone receptor (PR) positive, estrogen receptor (ER) positive breast cancer, and triple‐negative breast cancer (TNBC).
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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TNBC is the most aggressive type of breast cancer, and it is the leading cause of death in females aged 20–59 due to its metastatic nature .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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According to Gogate et al., the number of metastatic breast cancer cases is predicted to increase by 54.8% by 2030 in the United States .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Currently, pembrolizumab is the only cancer immunotherapy approved by the FDA to treat early‐stage TNBC .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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To meet the demand of these increasing metastatic breast cancer cases, there is a need to develop more effective and safe therapies that can help overcome TNBC .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Extracellular particles (EPs) are nanosized multimolecular bodies secreted by various cell types in the body that include but are not limited to extracellular vesicles (EVs) or vesicle‐like structures, according to the recent guidelines of the International Society of Extracellular Vesicles (ISEV) [6, 7].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The role of EPs is variable, though they are often considered cargo carriers that mediate cell‐to‐cell communication .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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EPs are composed of vesicular and non‐vesicular structures derived from the cells, and due to their natural ability to encapsulate and carry cellular materials like nucleic acids, proteins, chemokines, and cytokines, they can be leveraged as a potential candidate for cancer therapy.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The role of EPs in TNBC therapeutics is a topic of debate , especially since small EVs derived from TNBC cells can create an immunosuppressive environment by attacking critical immune cells like T cells and inducing apoptosis [10, 11].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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They have also been shown to affect the differentiation of monocytes into dendritic cells (DCs) and induce myeloid‐derived suppressor cells (MDSCs) [12, 13].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Immature MDSCs have been indicated to help tumors evade immune surveillance and make different cancer treatments ineffective [14, 15].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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On the other hand, small EVs derived from various immune cells, such as DCs, natural killer cells (NK cells), T cells, and B cells have shown anti‐cancer or pro‐tumorigenic properties .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Tumor progression has been linked with chronic inflammation and dysregulated activity of immune cells and is supported by a complex tumor microenvironment composed of different immune cells, extracellular matrix, non‐immune cells, and vascular structures.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Macrophages, a central cell type in tumor biology and immunology, play a crucial role in tumor progression or inhibition based on the signaling molecules they receive from the tumor microenvironment [18, 19].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Tumor‐derived EVs have been shown to change the fate of macrophage polarization, which determines the tumor‐inhibitory or tumor‐promoting effect of macrophage cells .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Researchers have found that breast cancer‐derived EVs can influence macrophages by regulating different pathways to support the tumor microenvironment [17, 20, 21].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Generally, macrophages polarized in the M1 phenotype (classically activated) indicate tissue inflammation, and the M2 phenotype (alternatively activated) creates an anti‐inflammatory environment.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The M1 phenotype is characterized by increased inducible nitric oxide (iNOS) synthase, an anti‐tumorigenic and inflammatory marker, while the M2 phenotype is more of a wound‐healing phenotype supporting tissue growth, cell migration, and metastasis via upregulation of arginase‐1 and CD‐206 molecules [22, 23].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Other papers have also detailed the role of tumor‐associated M2 macrophages, which have been associated with poor prognosis, chemoresistance, and metastasis [24, 25].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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EVs derived from M1 macrophages have been shown to exhibit the ability to transport a diverse array of chemokines, cytokines, and cellular proteins, demonstrating a potentially promising avenue for advancing TNBC treatment strategies [26, 27, 28].
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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For example, Baek et al. developed effective PEGylated M1 macrophage‐derived exosome mimetic nanovesicles (MNVs) to increase the accumulation of MNVs in the tumor.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Their research showed M1 macrophage‐derived exosome mimetic nanovesicles enhanced cancer‐targeting ability in a CT 26 tumor model .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Moreover, studies have demonstrated that when 4T1, a breast cancer tumor model, was targeted with docetaxel‐loaded M1‐derived EVs, it prompted the transformation of M0 macrophage phenotypes into the M1 phenotype within the tumor microenvironment .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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In another study, M1 macrophage‐derived exosomes were targeted against chemoresistance in pancreatic cancer.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The exosomes loaded with gemcitabine and deferasirox offer an excellent combination for therapeutic applications to potentially overcome chemoresistance .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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In addition to these studies, paclitaxel‐loaded M1 macrophages also showed the inhibition of 4T1 breast cancer cells .
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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To leverage the available literature and address current challenges in TNBC therapies, we aimed to explore the effect of M0, M1, and M2 macrophage‐derived EPs on TNBC.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Specifically, this study aimed to explore the potential effects of macrophage‐derived EPs on MDA‐MB‐231 cells.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Based on literature showing EVs exchange between cell types in the tumor microenvironment , we hypothesized that if cancer cell‐derived EVs can trigger M2 macrophages to support breast cancer tumor growth, we can use macrophage‐derived EPs to check their effect against TNBC.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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To test our hypothesis, EPs were isolated from RAW 264.7 cells stimulated with lipopolysaccharide (LPS) or interleukin‐4 (IL‐4) and categorized into M0, M1, and M2 macrophages (Figure 1).
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Experimental design schematic: 1.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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RAW 264.7 cells were grown in a 6‐well plate to compare M0, M1, and M2 stages.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The cells' M1 and M2 states were polarized using lipopolysaccharides (LPS) and interleukin (IL‐4) as stimuli, respectively.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The cells and collected cell culture media were subjected to characterization of polarization markers.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
2.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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RAW 264.7 cells were cultured in conditioned media that was fetal bovine serum (FBS)‐depleted to isolate and purify EPs from collected cell culture media in M0, M1, and M2 polarized states.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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All EPs were characterized after isolation and purification.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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3.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Isolated EPs were tested against MDA‐MB‐231 cells and caspase 3/7.
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PMC12217045
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
EP‐isolated conditioned media was added to MDA‐MB‐231 cells to differentiate between cell culture media effects from M0, M1, and M2 RAW 264.7 cells with M0, M1, and M2 isolated EPs.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
4.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
An XTT assay was performed to measure cell viability.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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The up arrows (↑) indicate increased proliferation and (↓) indicate decreased proliferation.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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Created with BioRender.com.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
RAW 264.7 macrophages (ATCC, USA) were cultured using Dulbecco's Modified Eagle Medium DMEM (Gibco, Cat #10569010) with 1% L‐glutamine (Gibco, Cat #25030081) and 10% heat‐inactivated FBS (Gibco, Cat #16140071) at 37°C and 5% CO2.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
MDA‐MB‐231 cells (ATCC, USA) were cultured using Dulbecco's Modified Eagle Medium DMEM (Gibco, Cat #10569010) with 1% L‐glutamine (Gibco, Cat #25030081) and 10% heat‐inactivated FBS (Gibco, Cat #16140071) at 37°C and 5% CO2.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
The cells were monitored and passaged when they reached 80% confluency.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
RAW 264.7 cells were seeded at a density of 4 × 10 cells per well in 6‐well plates to induce polarization into M1 and M2 phenotypes using lipopolysaccharide (LPS) (Thermo Fisher, USA) and mouse interleukin 4 (IL‐4) (eBioscience, Cat#BMS338), respectively.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
Polarization was induced based on a previously developed protocol .
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
Briefly, RAW 264.7 cells were stimulated with LPS and IL‐4 at the following concentrations: 0, 25, 50, and 100 ng/mL. Macrophages were incubated with inducing agents for 24 h, and polarization was verified under an Olympus IX51 bright‐field microscope.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
Images were taken using the SeBaView software and an external camera.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
To verify RAW 264.7 cells polarization, cells were seeded at a density of 4 × 10 per well in a 6‐well plate.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
The levels of pro‐inflammatory markers IL‐6 and TNF‐α were assessed using an IL‐6 mouse ELISA kit (Invitrogen, Cat#KMC0061) and a TNF‐α mouse ELISA kit (Invitrogen, Cat#BMS607‐3).
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
We followed the manufacturer's protocol to perform the assay.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
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All the reagents and standards were prepared at room temperature according to the protocol.
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
Next, 50 μL of cell culture media from M0 uninduced (Control), M1 LPS‐induced, and IL‐4‐induced M2 cells was collected to take the readings, and color change was measured using a multi‐mode microplate reader at a wavelength of 450 nm (Synergy MX).
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PMC12217045
|
M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.
|
RAW 264.7 cells at a density of 4 × 10 per well in a 6‐well plate were treated with LPS at different concentrations ranging from 0 to 100 ng/mL. After incubation for 24 h, cell culture media was collected to assess the presence of nitrites using a Griess reagent kit (Invitrogen, Cat#G7921), according to the manufacturer's protocol.
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