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fluorescence intensities  (Hitachi Ltd)


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    Hitachi Ltd fluorescence intensities
    Fluorescence Intensities, supplied by Hitachi Ltd, used in various techniques. Bioz Stars score: 99/100, based on 2320 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fluorescence intensities/product/Hitachi Ltd
    Average 99 stars, based on 2320 article reviews
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    Miltenyi Biotec propidium iodide fluorescence intensity
    A. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 TERT + cell lines on one hand and for the 3 ALT + cell lines on the other hand. For each cell line 1200 cells were seeded and proliferation was assessed at days 3, 4 and 5 (Fig. S10). Results presented here show the mean cell count on day 5 ± SD. Mann-Whitney test. ***: p < 0.001. B. Stacked bar chart presenting the result of three independent experiments in which cell fractions in G1, S and G2/M phases of the cell cycle were assessed using <t>propidium</t> iodide labelling for 2 TERT + hybrid cell lines and 3 ALT + cell lines. HBT3 TERT + cell line could not be analyzed because of the presence of two populations with different ploidies. Results correspond to the mean ± SD. Two-way ANOVA with Sidak’s correction for multiple comparisons test. **: p < 0.01 and ****: p < 0.0001. Individual data for each cell line are presented in Fig. S11. C. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 control cell lines (-DOX, in red) and for the 3 cell lines under DOX treatment (+DOX, in blue). Two shRNAs were used (sh2 & sh3). Results are mean ± SD. Unpaired t-test with Welch’s correction. No significant result. BLM inhibition induced by DOX treatment was assessed in parallel by real-time quantitative RT-PCR and western blot (Figs. S12A and S12B). Individual data for each cell line are presented in Fig. S12C.
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    Hitachi Ltd fluorescence intensities
    A. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 TERT + cell lines on one hand and for the 3 ALT + cell lines on the other hand. For each cell line 1200 cells were seeded and proliferation was assessed at days 3, 4 and 5 (Fig. S10). Results presented here show the mean cell count on day 5 ± SD. Mann-Whitney test. ***: p < 0.001. B. Stacked bar chart presenting the result of three independent experiments in which cell fractions in G1, S and G2/M phases of the cell cycle were assessed using <t>propidium</t> iodide labelling for 2 TERT + hybrid cell lines and 3 ALT + cell lines. HBT3 TERT + cell line could not be analyzed because of the presence of two populations with different ploidies. Results correspond to the mean ± SD. Two-way ANOVA with Sidak’s correction for multiple comparisons test. **: p < 0.01 and ****: p < 0.0001. Individual data for each cell line are presented in Fig. S11. C. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 control cell lines (-DOX, in red) and for the 3 cell lines under DOX treatment (+DOX, in blue). Two shRNAs were used (sh2 & sh3). Results are mean ± SD. Unpaired t-test with Welch’s correction. No significant result. BLM inhibition induced by DOX treatment was assessed in parallel by real-time quantitative RT-PCR and western blot (Figs. S12A and S12B). Individual data for each cell line are presented in Fig. S12C.
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    Hitachi Ltd fluorescence intensity
    A. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 TERT + cell lines on one hand and for the 3 ALT + cell lines on the other hand. For each cell line 1200 cells were seeded and proliferation was assessed at days 3, 4 and 5 (Fig. S10). Results presented here show the mean cell count on day 5 ± SD. Mann-Whitney test. ***: p < 0.001. B. Stacked bar chart presenting the result of three independent experiments in which cell fractions in G1, S and G2/M phases of the cell cycle were assessed using <t>propidium</t> iodide labelling for 2 TERT + hybrid cell lines and 3 ALT + cell lines. HBT3 TERT + cell line could not be analyzed because of the presence of two populations with different ploidies. Results correspond to the mean ± SD. Two-way ANOVA with Sidak’s correction for multiple comparisons test. **: p < 0.01 and ****: p < 0.0001. Individual data for each cell line are presented in Fig. S11. C. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 control cell lines (-DOX, in red) and for the 3 cell lines under DOX treatment (+DOX, in blue). Two shRNAs were used (sh2 & sh3). Results are mean ± SD. Unpaired t-test with Welch’s correction. No significant result. BLM inhibition induced by DOX treatment was assessed in parallel by real-time quantitative RT-PCR and western blot (Figs. S12A and S12B). Individual data for each cell line are presented in Fig. S12C.
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    Sartorius AG fluorescent caspase 3 7 signal intensity
    TfR1 binding and TNFα inhibitory activity of optimized and humanized heterodimers. a Schematic representation of the 16 humanized and optimized TNFI–TfR1b heterodimers. b Flow cytometry analysis in HEK293 cells stably expressing human TfR1, comparing the binding of heterodimers to that of their parental humanized TfR1b-Nbs. c ) Dose–response apoptosis inhibition curves in WEHI-13VAR cells treated with human TNFα and twofold serial dilutions of TNFI–TfR1b heterodimers (100,000 to 12.21 pM). Apoptosis was measured using <t>a</t> <t>fluorogenic</t> <t>caspase-3/7</t> activation assay. Caspase-3/7 activity in the TNFα-only samples was defined as 100%. The IC₅₀ values of the heterodimers were comparable to those of the parental humanized nanobodies TNFI-α (IC₅₀ = 48.84 pM, range: 42.11–56.56) and TNFI-β (IC₅₀ = 64.31 pM, range: 57.17–72.31).). Data are presented as mean ± SEM from triplicate measurements and were analyzed using the
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    ( A ). Representative images of OE-19 xenograft bearing mice imaged at 4 and 6 h post NF-800 injection at IVIS Spectrum. ( B ) Mean <t>fluorescence</t> intensity values of Tumor, Kidney and Liver of animals bearing OE-19 xenografts and treated with NF-800. ( C ) Lifetime values obtained with tail fitting of the abovementioned tissues, compared to the probe dissolved in PBS (n = 7 animals). One way ANOVA Multiple comparison test (* = p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001).
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    ( A ) Schematic representation of the experimental approach used to test whether senescent cell–derived small extracellular vesicles and particles (EVPs) can be taken up by proliferating cells. Proliferating IMR90 cells were treated with PKH67, a green <t>fluorescent</t> lipophilic membrane dye, alone or with PKH67-labeled EVPs isolated from senescent cells. ( B ) Representative immunofluorescence images of proliferating cells treated with or without PKH67-labeled sEVP fractions from senescent cells, using different sEVP volumes while keeping the PKH67 lipid dye concentration unchanged. Boxes indicate expanded region and arrows indicate PKH67 puncta in recipient cells. ( C ) Quantification of internalized PKH67-labeled sEVPs by proliferating cells. Data are presented as mean ± SD (n=3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.023, **p=0.0010, ****p<0.0001. ( D ) Schematic representation of the experimental setup: proliferating IMR90 cells were treated with no sEVPs or sEVPs secreted by proliferating cells treated with DMSO, or senescent cells treated with the inhibitor of CCF formation, MDM2 inhibitor RG7388 (MDM2i) or DMSO vehicle. ( E ) Quantification of cGAMP concentration in proliferating cells treated with no sEVPs or sEVPs (40 μL) from proliferating cells treated with DMSO, or senescent cells treated with MDM2i or DMSO vehicle. sEVPs were isolated from equivalent numbers of cells for each condition and resuspended in identical buffer volumes. Data are presented as mean ± SD (n = 3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.011, **p=0.0094.
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    ( A ) Schematic representation of the experimental approach used to test whether senescent cell–derived small extracellular vesicles and particles (EVPs) can be taken up by proliferating cells. Proliferating IMR90 cells were treated with PKH67, a green <t>fluorescent</t> lipophilic membrane dye, alone or with PKH67-labeled EVPs isolated from senescent cells. ( B ) Representative immunofluorescence images of proliferating cells treated with or without PKH67-labeled sEVP fractions from senescent cells, using different sEVP volumes while keeping the PKH67 lipid dye concentration unchanged. Boxes indicate expanded region and arrows indicate PKH67 puncta in recipient cells. ( C ) Quantification of internalized PKH67-labeled sEVPs by proliferating cells. Data are presented as mean ± SD (n=3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.023, **p=0.0010, ****p<0.0001. ( D ) Schematic representation of the experimental setup: proliferating IMR90 cells were treated with no sEVPs or sEVPs secreted by proliferating cells treated with DMSO, or senescent cells treated with the inhibitor of CCF formation, MDM2 inhibitor RG7388 (MDM2i) or DMSO vehicle. ( E ) Quantification of cGAMP concentration in proliferating cells treated with no sEVPs or sEVPs (40 μL) from proliferating cells treated with DMSO, or senescent cells treated with MDM2i or DMSO vehicle. sEVPs were isolated from equivalent numbers of cells for each condition and resuspended in identical buffer volumes. Data are presented as mean ± SD (n = 3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.011, **p=0.0094.
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    ( A ) Schematic representation of the experimental approach used to test whether senescent cell–derived small extracellular vesicles and particles (EVPs) can be taken up by proliferating cells. Proliferating IMR90 cells were treated with PKH67, a green <t>fluorescent</t> lipophilic membrane dye, alone or with PKH67-labeled EVPs isolated from senescent cells. ( B ) Representative immunofluorescence images of proliferating cells treated with or without PKH67-labeled sEVP fractions from senescent cells, using different sEVP volumes while keeping the PKH67 lipid dye concentration unchanged. Boxes indicate expanded region and arrows indicate PKH67 puncta in recipient cells. ( C ) Quantification of internalized PKH67-labeled sEVPs by proliferating cells. Data are presented as mean ± SD (n=3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.023, **p=0.0010, ****p<0.0001. ( D ) Schematic representation of the experimental setup: proliferating IMR90 cells were treated with no sEVPs or sEVPs secreted by proliferating cells treated with DMSO, or senescent cells treated with the inhibitor of CCF formation, MDM2 inhibitor RG7388 (MDM2i) or DMSO vehicle. ( E ) Quantification of cGAMP concentration in proliferating cells treated with no sEVPs or sEVPs (40 μL) from proliferating cells treated with DMSO, or senescent cells treated with MDM2i or DMSO vehicle. sEVPs were isolated from equivalent numbers of cells for each condition and resuspended in identical buffer volumes. Data are presented as mean ± SD (n = 3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.011, **p=0.0094.
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    A. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 TERT + cell lines on one hand and for the 3 ALT + cell lines on the other hand. For each cell line 1200 cells were seeded and proliferation was assessed at days 3, 4 and 5 (Fig. S10). Results presented here show the mean cell count on day 5 ± SD. Mann-Whitney test. ***: p < 0.001. B. Stacked bar chart presenting the result of three independent experiments in which cell fractions in G1, S and G2/M phases of the cell cycle were assessed using propidium iodide labelling for 2 TERT + hybrid cell lines and 3 ALT + cell lines. HBT3 TERT + cell line could not be analyzed because of the presence of two populations with different ploidies. Results correspond to the mean ± SD. Two-way ANOVA with Sidak’s correction for multiple comparisons test. **: p < 0.01 and ****: p < 0.0001. Individual data for each cell line are presented in Fig. S11. C. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 control cell lines (-DOX, in red) and for the 3 cell lines under DOX treatment (+DOX, in blue). Two shRNAs were used (sh2 & sh3). Results are mean ± SD. Unpaired t-test with Welch’s correction. No significant result. BLM inhibition induced by DOX treatment was assessed in parallel by real-time quantitative RT-PCR and western blot (Figs. S12A and S12B). Individual data for each cell line are presented in Fig. S12C.

    Journal: bioRxiv

    Article Title: Alternative Lengthening of Telomeres and CINSARC are interconnected toward non-translocation-related sarcomas progression

    doi: 10.64898/2026.01.23.701253

    Figure Lengend Snippet: A. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 TERT + cell lines on one hand and for the 3 ALT + cell lines on the other hand. For each cell line 1200 cells were seeded and proliferation was assessed at days 3, 4 and 5 (Fig. S10). Results presented here show the mean cell count on day 5 ± SD. Mann-Whitney test. ***: p < 0.001. B. Stacked bar chart presenting the result of three independent experiments in which cell fractions in G1, S and G2/M phases of the cell cycle were assessed using propidium iodide labelling for 2 TERT + hybrid cell lines and 3 ALT + cell lines. HBT3 TERT + cell line could not be analyzed because of the presence of two populations with different ploidies. Results correspond to the mean ± SD. Two-way ANOVA with Sidak’s correction for multiple comparisons test. **: p < 0.01 and ****: p < 0.0001. Individual data for each cell line are presented in Fig. S11. C. The bar chart corresponds to the mean of three independent proliferation experiments for the 3 control cell lines (-DOX, in red) and for the 3 cell lines under DOX treatment (+DOX, in blue). Two shRNAs were used (sh2 & sh3). Results are mean ± SD. Unpaired t-test with Welch’s correction. No significant result. BLM inhibition induced by DOX treatment was assessed in parallel by real-time quantitative RT-PCR and western blot (Figs. S12A and S12B). Individual data for each cell line are presented in Fig. S12C.

    Article Snippet: DNA content was quantified with propidium iodide fluorescence intensity by flow cytometry (MACSQuant VYB, Miltenyi Biotec) and analyzed using the cycle tool of the FlowJo software (RRID:SCR_008520, v10.10.0, FlowJo LLC) and GraphPad Prism (RRID:SCR_002798, v6.01, GraphPad Software Inc.) software.

    Techniques: Cell Characterization, MANN-WHITNEY, Control, Inhibition, Quantitative RT-PCR, Western Blot

    TfR1 binding and TNFα inhibitory activity of optimized and humanized heterodimers. a Schematic representation of the 16 humanized and optimized TNFI–TfR1b heterodimers. b Flow cytometry analysis in HEK293 cells stably expressing human TfR1, comparing the binding of heterodimers to that of their parental humanized TfR1b-Nbs. c ) Dose–response apoptosis inhibition curves in WEHI-13VAR cells treated with human TNFα and twofold serial dilutions of TNFI–TfR1b heterodimers (100,000 to 12.21 pM). Apoptosis was measured using a fluorogenic caspase-3/7 activation assay. Caspase-3/7 activity in the TNFα-only samples was defined as 100%. The IC₅₀ values of the heterodimers were comparable to those of the parental humanized nanobodies TNFI-α (IC₅₀ = 48.84 pM, range: 42.11–56.56) and TNFI-β (IC₅₀ = 64.31 pM, range: 57.17–72.31).). Data are presented as mean ± SEM from triplicate measurements and were analyzed using the

    Journal: Cell Communication and Signaling : CCS

    Article Title: The NewroBus platform: engineered humanized anti-TfR1 nanobodies for efficient brain delivery

    doi: 10.1186/s12964-025-02605-1

    Figure Lengend Snippet: TfR1 binding and TNFα inhibitory activity of optimized and humanized heterodimers. a Schematic representation of the 16 humanized and optimized TNFI–TfR1b heterodimers. b Flow cytometry analysis in HEK293 cells stably expressing human TfR1, comparing the binding of heterodimers to that of their parental humanized TfR1b-Nbs. c ) Dose–response apoptosis inhibition curves in WEHI-13VAR cells treated with human TNFα and twofold serial dilutions of TNFI–TfR1b heterodimers (100,000 to 12.21 pM). Apoptosis was measured using a fluorogenic caspase-3/7 activation assay. Caspase-3/7 activity in the TNFα-only samples was defined as 100%. The IC₅₀ values of the heterodimers were comparable to those of the parental humanized nanobodies TNFI-α (IC₅₀ = 48.84 pM, range: 42.11–56.56) and TNFI-β (IC₅₀ = 64.31 pM, range: 57.17–72.31).). Data are presented as mean ± SEM from triplicate measurements and were analyzed using the "Inhibitor vs. Normalized Response" model in GraphPad Prism 10 software

    Article Snippet: Plates were immediately placed in the Incucyte Live-Cell Imaging System (Sartorius), and fluorescent signals were monitored every 2–4 h for up to 24 h. Fluorescent caspase-3/7 signal intensity was quantified using Incucyte analysis software.

    Techniques: Binding Assay, Activity Assay, Flow Cytometry, Stable Transfection, Expressing, Inhibition, Activation Assay, Software

    ( A ). Representative images of OE-19 xenograft bearing mice imaged at 4 and 6 h post NF-800 injection at IVIS Spectrum. ( B ) Mean fluorescence intensity values of Tumor, Kidney and Liver of animals bearing OE-19 xenografts and treated with NF-800. ( C ) Lifetime values obtained with tail fitting of the abovementioned tissues, compared to the probe dissolved in PBS (n = 7 animals). One way ANOVA Multiple comparison test (* = p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001).

    Journal: Scientific Reports

    Article Title: Investigating probe-receptor interactions and enhancing fluorescence guided surgery with fluorescence lifetime imaging and NF-800 in HER-2 positive esophageal adenocarcinoma

    doi: 10.1038/s41598-025-31872-8

    Figure Lengend Snippet: ( A ). Representative images of OE-19 xenograft bearing mice imaged at 4 and 6 h post NF-800 injection at IVIS Spectrum. ( B ) Mean fluorescence intensity values of Tumor, Kidney and Liver of animals bearing OE-19 xenografts and treated with NF-800. ( C ) Lifetime values obtained with tail fitting of the abovementioned tissues, compared to the probe dissolved in PBS (n = 7 animals). One way ANOVA Multiple comparison test (* = p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001).

    Article Snippet: Fluorescence intensity acquisitions were performed at IVIS Spectrum (Perkin Elmer Italia S.p.A.) equipped with an excitation filter at 745 nm and emission filter at 800 nm with 30 nm and 20 nm bandwidth, respectively.

    Techniques: Injection, Fluorescence, Comparison

    ( A ) Fluorescence intensity values (counts) and respective lifetimes (ns) of ex vivo tumor and kidneys 6 h after administration of NF-800. ( B ) Fluorescence intensity values and respective lifetimes (ns) of ex vivo tumor and liver after administration of Tz-800. (One way ANOVA Multiple comparison test was performed between all the groups (e.g. tumor vs kidney; tumor vs PBS; kidney vs PBS) (* = p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001).

    Journal: Scientific Reports

    Article Title: Investigating probe-receptor interactions and enhancing fluorescence guided surgery with fluorescence lifetime imaging and NF-800 in HER-2 positive esophageal adenocarcinoma

    doi: 10.1038/s41598-025-31872-8

    Figure Lengend Snippet: ( A ) Fluorescence intensity values (counts) and respective lifetimes (ns) of ex vivo tumor and kidneys 6 h after administration of NF-800. ( B ) Fluorescence intensity values and respective lifetimes (ns) of ex vivo tumor and liver after administration of Tz-800. (One way ANOVA Multiple comparison test was performed between all the groups (e.g. tumor vs kidney; tumor vs PBS; kidney vs PBS) (* = p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001).

    Article Snippet: Fluorescence intensity acquisitions were performed at IVIS Spectrum (Perkin Elmer Italia S.p.A.) equipped with an excitation filter at 745 nm and emission filter at 800 nm with 30 nm and 20 nm bandwidth, respectively.

    Techniques: Fluorescence, Ex Vivo, Comparison

    Representative Fluorescence Intensity (AU) and FLT parametric map (ns) of a tumor treated with NF-800. ROIs indicate tumors, which appears to have spread throughout the stomach. Histogram represents distribution of lifetimes across pixels, as fitted to obtain the parametric map.

    Journal: Scientific Reports

    Article Title: Investigating probe-receptor interactions and enhancing fluorescence guided surgery with fluorescence lifetime imaging and NF-800 in HER-2 positive esophageal adenocarcinoma

    doi: 10.1038/s41598-025-31872-8

    Figure Lengend Snippet: Representative Fluorescence Intensity (AU) and FLT parametric map (ns) of a tumor treated with NF-800. ROIs indicate tumors, which appears to have spread throughout the stomach. Histogram represents distribution of lifetimes across pixels, as fitted to obtain the parametric map.

    Article Snippet: Fluorescence intensity acquisitions were performed at IVIS Spectrum (Perkin Elmer Italia S.p.A.) equipped with an excitation filter at 745 nm and emission filter at 800 nm with 30 nm and 20 nm bandwidth, respectively.

    Techniques: Fluorescence

    ( A ) Schematic representation of the experimental approach used to test whether senescent cell–derived small extracellular vesicles and particles (EVPs) can be taken up by proliferating cells. Proliferating IMR90 cells were treated with PKH67, a green fluorescent lipophilic membrane dye, alone or with PKH67-labeled EVPs isolated from senescent cells. ( B ) Representative immunofluorescence images of proliferating cells treated with or without PKH67-labeled sEVP fractions from senescent cells, using different sEVP volumes while keeping the PKH67 lipid dye concentration unchanged. Boxes indicate expanded region and arrows indicate PKH67 puncta in recipient cells. ( C ) Quantification of internalized PKH67-labeled sEVPs by proliferating cells. Data are presented as mean ± SD (n=3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.023, **p=0.0010, ****p<0.0001. ( D ) Schematic representation of the experimental setup: proliferating IMR90 cells were treated with no sEVPs or sEVPs secreted by proliferating cells treated with DMSO, or senescent cells treated with the inhibitor of CCF formation, MDM2 inhibitor RG7388 (MDM2i) or DMSO vehicle. ( E ) Quantification of cGAMP concentration in proliferating cells treated with no sEVPs or sEVPs (40 μL) from proliferating cells treated with DMSO, or senescent cells treated with MDM2i or DMSO vehicle. sEVPs were isolated from equivalent numbers of cells for each condition and resuspended in identical buffer volumes. Data are presented as mean ± SD (n = 3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.011, **p=0.0094.

    Journal: bioRxiv

    Article Title: Senescent cells secrete chromatin components via senescence-associated extracellular particles

    doi: 10.64898/2025.12.12.694055

    Figure Lengend Snippet: ( A ) Schematic representation of the experimental approach used to test whether senescent cell–derived small extracellular vesicles and particles (EVPs) can be taken up by proliferating cells. Proliferating IMR90 cells were treated with PKH67, a green fluorescent lipophilic membrane dye, alone or with PKH67-labeled EVPs isolated from senescent cells. ( B ) Representative immunofluorescence images of proliferating cells treated with or without PKH67-labeled sEVP fractions from senescent cells, using different sEVP volumes while keeping the PKH67 lipid dye concentration unchanged. Boxes indicate expanded region and arrows indicate PKH67 puncta in recipient cells. ( C ) Quantification of internalized PKH67-labeled sEVPs by proliferating cells. Data are presented as mean ± SD (n=3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.023, **p=0.0010, ****p<0.0001. ( D ) Schematic representation of the experimental setup: proliferating IMR90 cells were treated with no sEVPs or sEVPs secreted by proliferating cells treated with DMSO, or senescent cells treated with the inhibitor of CCF formation, MDM2 inhibitor RG7388 (MDM2i) or DMSO vehicle. ( E ) Quantification of cGAMP concentration in proliferating cells treated with no sEVPs or sEVPs (40 μL) from proliferating cells treated with DMSO, or senescent cells treated with MDM2i or DMSO vehicle. sEVPs were isolated from equivalent numbers of cells for each condition and resuspended in identical buffer volumes. Data are presented as mean ± SD (n = 3 independent experiments). Statistical significance was determined using two-sided one-way ANOVA: *p=0.011, **p=0.0094.

    Article Snippet: The same channel thresholds were maintained for all cells, and the most intense fluorescent overlap was quantified by Imaris as voxels (i.e., overlap between volumetric pixels in either channel).

    Techniques: Derivative Assay, Membrane, Labeling, Isolation, Immunofluorescence, Concentration Assay