Fig. 5
From: Deletion of MAPL ameliorates septic cardiomyopathy by mitigating mitochondrial dysfunction
MAPL knockout or knockdown suppressed CLP or LPS-induced increase of drp1 in heart tissues and H9C2 cardiomyocytes. A. The protein levels of drp1 and mfn2 in heart tissue of mice were determined by westernblot (*P < 0.05, **P < 0.01, n = 5 for each group). B. The protein levels of drp1 and mfn2 in H9C2 cardiomyocyte were determined by westernblot (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n = 6 repeated experiments). C. The expression of drp1 in mitochondria of heart tissues from WT or CKO mice after sham surgery or CLP was detected by western blot (***P < 0.001, ****P < 0.0001, n = 5 for each group). D. The expression of drp1in mitochondria of shNC- and shMAPL-cardiomyocytes after LPS (20 µg/ml) treatment was detected by western blot (*P < 0.05, **P < 0.01, n = 5 repeated experiments). E. Immunofluorescence staining was performed to detect the expression of mitochondrial fragment in shNC- and shMAPL-cardiomyocytes after LPS (20 µg/ml) treatment (scale bar = 10 μm. n = 5 repeated experiments)