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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a <t>fluorescence-based</t> <t>oxygen-consumption</t> assay. <t>OCR</t> profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.
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MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a fluorescence-based oxygen-consumption assay. OCR profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.

Journal: Redox Report : Communications in Free Radical Research

Article Title: Coordinated mitochondrial quality control underlies oxidative stress resilience in MUSE stem cells

doi: 10.1080/13510002.2026.2698189

Figure Lengend Snippet: MUSE cells preserve mitochondrial respiratory function and membrane potential under oxidative stress (A) Mitochondrial respiratory activity was evaluated 24 h after H₂O₂ exposure using a fluorescence-based oxygen-consumption assay. OCR profiles were obtained following sequential treatment with oligomycin, FCCP, and rotenone. Histograms summarize basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. (B) Mitochondrial membrane potential (ΔΨm) was assessed by flow cytometry at baseline, 1 h, and 24 h after oxidative stress. The bar graph summarizes the percentage of cells with polarized mitochondria. As controls, CCCP-treated cells were used as the positive control (loss of polarization), whereas unstained cells served as the negative control. All data are presented as mean ± SD (n = 3 from independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001 vs. respective untreated controls; ###p < 0.001 vs. MSCs + H₂O₂.

Article Snippet: Mitochondrial respiratory activity was evaluated using an Enhanced Oxygen Consumption Rate (OCR) Fluorometric Assay Kit (Elabscience E-BC-F070) performed in 96-well plates according to the manufacturer's instructions.

Techniques: Membrane, Activity Assay, Fluorescence, Flow Cytometry, Positive Control, Negative Control