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mouse anti mmp 1  (Developmental Studies Hybridoma Bank)
94
Developmental Studies Hybridoma Bank mouse anti mmp 1
Mouse Anti Mmp 1, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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jc 1 mmp assay kit  (MedChemExpress)
96
MedChemExpress jc 1 mmp assay kit
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Jc 1 Mmp Assay Kit, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mmp 13  (Proteintech)
96
Proteintech mmp 13
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Mmp 13, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mitochondrial membrane potential mmp assay  (MedChemExpress)
96
MedChemExpress mitochondrial membrane potential mmp assay
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Mitochondrial Membrane Potential Mmp Assay, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mmp 2  (Proteintech)
96
Proteintech mmp 2
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Mmp 2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mmp 12  (Proteintech)
95
Proteintech mmp 12
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Mmp 12, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human mmp-1 elisa kit  (Multi Sciences (Lianke) Biotech Co Ltd)
93
Multi Sciences (Lianke) Biotech Co Ltd human mmp-1 elisa kit
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Human Mmp 1 Elisa Kit, supplied by Multi Sciences (Lianke) Biotech Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit mab cell signaling technology mmp3 polyclonal antibody proteintech mmp 9 n terminal  (Proteintech)
96
Proteintech rabbit mab cell signaling technology mmp3 polyclonal antibody proteintech mmp 9 n terminal
Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H <t>)</t> <t>JC-1</t> aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
Rabbit Mab Cell Signaling Technology Mmp3 Polyclonal Antibody Proteintech Mmp 9 N Terminal, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H ) JC-1 aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Metabolic reprogramming and enhanced mitochondrial function in LPS-activated macrophages in response to LEV Tet−PKM2 @TA treatment. The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) Heatmap representing differentially detected metabolites involved in glycolysis and the TCA cycle in the Control, LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA groups ( n = 4). ( B ) Concentrations of key glycolysis and TCA metabolites in Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( C ) Schematic illustration revealing changes in key glycolysis and TCA metabolites in the LEVs Tet−PKM2 @TA group versus the Control group. The up (down) arrows indicate increased (decreased) levels of metabolites in macrophages. ( D ) Kinetic profile of the ECAR in LPS-activated macrophages in response to sequential injections of glucose, oligomycin, and 2-DG in various groups (Seahorse XF test) ( n = 4). ( E ) Quantification of glycolysis, glycolytic capacity and glycolytic reserve in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( F ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 4). ( G ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( H ) JC-1 aggregation (red fluorescence) in healthy mitochondria and cytosolic JC-1 monomers in compromised mitochondria (green fluorescence) (immunofluorescence assays). ( I ) Quantitative analysis of MMP levels determined by the relative ratio of red/green fluorescence intensity in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 4). ( J ) Intracellular ATP levels of LPS-activated macrophages in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). ( K-M ) The macrophages were pretreated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 10 μM UK-5099, 100 μg/mL LEVs Tet−PKM2 @TA, or 10 μM UK-5099 plus 100 μg/mL LEVs Tet−PKM2 @TA for another 24 h. ( K ) Schematic illustration revealing mechanism of LEVs Tet−PKM2 @TA promotes macrophage metabolic reprogramming depending on pyruvate influx into the TCA cycle. ( L ) Kinetic profile of the OCR in LPS-activated macrophages in response to sequential injections of oligomycin, FCCP, and Rot/AA in various groups (Seahorse XF test) ( n = 3). ( M ) Quantification of basal respiration, ATP production, and maximal respiration in the Control, UK-5099, LEVs Tet−PKM2 @TA, and UK-5099 + LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( B , E , G, I, J , and M ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Article Snippet: The MMP of the macrophages was assessed using a JC-1 MMP Assay Kit (MCE).

Techniques: Control, Fluorescence, Immunofluorescence