Fig. 4: Knockout of Psmb8 accelerates I/R-induced cardiac dysfunction and injury. | Cell Death & Disease

Fig. 4: Knockout of Psmb8 accelerates I/R-induced cardiac dysfunction and injury.

From: Psmb8 inhibits mitochondrial fission and alleviates myocardial ischaemia/reperfusion injury by targeting Drp1 degradation

Fig. 4

A Male WT and Psmb8-KO mice were exposed to I/R or sham conditions for 24 h. Echocardiographic examination of the left ventricle (LV) (left) and percentages of the ejection fraction (EF) and fraction shortening (FS) (right, n = 6) are shown. B Images of heart sections stained with TTC and Evans blue dye (left). Percentages of the area at risk (AAR) to the LV area or the infarct area to the LV area (right, n = 6). Bar: 2.5 mm. C Images of heart sections stained with TUNEL (red), anti-α-actinin (green) and DAPI (blue) (top, left) and the percentages of TUNEL-positive nuclei (middle, n = 6). Heart sections were stained with DHE dye (bottom, left), and ROS concentrations were quantified (right, n = 6). Bar: 50 μm. D Immunoblot analysis of Bcl-2, Bax and cleaved caspase-3 protein levels (left) and quantification (right, n = 4). E Mitochondrial morphology in cardiomyocytes was analysed by transmission electron microscopy (left). Bar: 1 µm. Red arrows indicate fragmented mitochondria. Quantification of fragmented mitochondria (right, n = 3). F qPCR analysis of NADH dehydrogenase subunit 1 to determine changes in mitochondrial (mt) DNA copy numbers in the heart. The β-globin gene was used as the control. G ATP levels in the heart were measured (n = 6). H The protein levels of total Drp1, p-Drp1 (S616), Mfn1, and Mfn2 in the heart were examined by immunoblot analysis (left), and the levels of these proteins were quantified (right, n = 4). The values are expressed as the mean ± SEM, and n indicates the sample number per group.

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