The DNA-dependent protein kinase catalytic subunit promotes sepsis-induced cardiac dysfunction through disrupting INF-2-dependent mitochondrial dynamics

Figures

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  Figure 1. DNA-PKcs knockdown alleviates LPS-mediated cardiomyocyte death and dysfunction. A. MTT assay was used to evaluate the cell viability of HL-1 cells in the presence of LPS. shRNA against DNA-PKcs was transfected into HL-1 cells before LPS treatment. B. CCK-8 assay was applied to analyze the cell viability of HL-1 cells upon LPS exposure. shRNA against DNA-PKcs was transfected into HL-1 cells before LPS treatment. C-D. ELISA kits were used to analyze the activities of caspase-3 and caspase-9 in the presence of LPS. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.

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  Figure 2. DNA-PKcs knockdown attenuates LPS-caused mitochondrial dysfunction. A. ATP production was determined by ELISA. B-D. The activities of mitochondrial respiratory complex I, II, III were measured by ELISA. E. Mitochondrial potential was evaluated through immunofluorescence assay and the relative changes of mitochondrial potential was evaluated. F. The mPTP opening rate was determined by an ELIST kit. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.

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  Figure 3. DNA-PKcs knockdown attenuates LPS-caused mitochondrial dynamics disorder through affecting INF2 expression. A-F. RNA was isolated from HL-1 cells and the transcriptions of Drp1, Fis1, Mff, Mfn1, Mfn2 and Opa1 were measured by qPCR. G. Proteins were collected from HL-1 cells and the expression of INF2 was measured by western blots. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.

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  Figure 4. INF2 knockdown attenuates LPS-caused mitochondrial dynamics disorder. A-F. RNA was isolated from HL-1 cells and the transcriptions of Drp1, Fis1, Mff, Mfn1, Mfn2 and Opa1 were measured by qPCR. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.

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  Figure 5. INF2 knockdown attenuates LPS-caused mitochondrial dysfunction. A. ATP production was determined by ELISA. B-D. The activities of mitochondrial respiratory complex I, II, III were measured by ELISA. E. Mitochondrial potential was evaluated through immunofluorescence assay and the relative changes of mitochondrial potential was evaluated. F. The mPTP opening rate was determined by an ELIST kit. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.

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  Figure 6. INF2 knockdown reduces LPS-mediated cardiomyocyte dysfunction and death. A. MTT assay was used to evaluate the cell viability of HL-1 cells in the presence of LPS. shRNA against INF2 was transfected into HL-1 cells before LPS treatment. B. CCK-8 assay was applied to analyze the cell viability of HL-1 cells upon LPS exposure. shRNA against INF2 was transfected into HL-1 cells before LPS treatment. C-D. ELISA kits were used to analyze the activities of caspase-3 and caspase-9 in the presence of LPS. *p<0.05 vs. PBS+sh-Ctrl group, #p<0.05 vs. LPS+sh-Ctrl group.