TLR4-SIRT3 Mechanism Modulates Mitochondrial and Redox Homeostasis and Promotes EPCs Recruitment and Survival

Figure 2

LPS induces mitochondrial permeability through TLR4. High-dose LPS (10 μg/mL) treatment induced mitochondrial dysfunction via prolonged mPTP activation in EPCs, which can be ameliorated by TLR4-specific blocker TAK-242 or SIRT3 overexpression (LetSIRT3). (a) Representative fluorescent images with calcein staining (green) and (b) quantitative analysis of fluorescence intensity are shown here ( per group, results were expressed as ). Cell nuclei are stained by DAPI. (Scale bars 100 μm). vs. control; vs. 1 μg/mL LPS vs. 10 μg/mL LPS. (c) The western blot assay demonstrated the efficiency of siRNA-induced knock down or lentiviral transfection-induced overexpression of SIRT3 in EPCs (). vs. control; vs. LetSIRT3 group.

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