Abstract
Purpose: The concept that the failing heart is energy starved is supported by observations of abnormal energy production by the mitochondria respiratory chain. We previously showed that the physiologic processes of mitochondria biogenesis, fission and fusion are abnormal in the failing human heart and give rise to mitochondria hyperplasia, reduced organelle size and poor respiration. This study examined the regulation of two key mitochondrial proteins; porin (PO), the outer membrane protein that forms the aqueous channel for metabolite flux between mitochondria and cytosol, and mitofilin (MF), a critical organizer of mitochondria cristae morphology and thus indispensible for normal mitochondrial function. Methods and Materials: Studies were performed in LV tissue homogenate obtained from 6 normal (NL) donor human hearts, 6 explanted failing human hearts with dilated cardiomyopathy (DCM) and 6 explanted failing human hearts with ischemic cardiomyopathy (ICM). Protein expression of PO, MF and glyceraldehyde 3-phosphate dehydrogenase (GAPDH), a housekeeping protein, was measured with specific antibodies and Western blotting and bands quantified in densitometric units (du). Results: Compared to NL donor hearts, MF was significantly reduced in ICM and DCM hearts while expression of PO and GAPDH were unchanged (Table).
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