Fig. 3: Overexpression of Psmb8 in cardiomyocytes blocks I/R-induced myocardial mitochondrial dynamic imbalance and dysfunction. | Cell Death & Disease

Fig. 3: Overexpression of Psmb8 in cardiomyocytes blocks I/R-induced myocardial mitochondrial dynamic imbalance and dysfunction.

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

Fig. 3

A Heatmap of 268 differentially expressed proteins (DEPs) identified by LC–MS/MS between WT and rAAV9-Psmb8-injected mice after sham or I/R injury (n = 5 per group). Red: upregulated; blue: downregulated. B Gene Ontology (GO) functional enrichment analysis of the upregulated proteins in rAAV9-Psmb8-injected hearts. C Wikipathway analysis of the upwnregulated proteins in rAAV9-Psmb8 hearts. D Evaluation of mitochondrial morphology in cardiomyocytes using transmission electron microscopy (left). Bar: 1 µm. Red arrows indicate fragmented mitochondria. Quantification of fragmented mitochondria (right, n = 3). E qPCR analysis of NADH dehydrogenase subunit 1 to determine the mtDNA copy number per cell in the heart. The β-globin gene was used as the control. F Analysis of ATP levels in the hearts were measured (n = 6). G 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.

Back to article page