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Department of Pediatrics, University of Iowa, Iowa City, Iowa 52242
Developmental downregulation of the malate-aspartate shuttle has
been observed in cardiac mitochondria. The goals of this study were to
determine the time course of the postnatal decline and to identify
potential regulatory sites by measuring steady-state myocardial mRNA
and protein levels of the mitochondrial proteins involved in the
shuttle. By use of isolated porcine cardiac mitochondria incubated with
saturating concentrations of the cytosolic components of the
malate-aspartate shuttle, shuttle capacity was found to decline by
~50% during the first 5 wk of life (from 921 ± 48 to 531 ± 53 nmol · min
1 · mg
protein1). Mitochondrial
aspartate aminotransferase mRNA levels were greater in adult than in
newborn myocardium. mRNA levels of mitochondrial malate dehydrogenase
in adult cardiac tissue were 224% of levels in newborn tissue, whereas
protein levels were 54% greater in adult myocardium.
Aspartate/glutamate carrier protein levels were also greater in adult
than in newborn tissue. mRNA and protein levels of the
oxoglutarate/malate carrier were increased in newborn myocardium. It
was concluded that 1) myocardial
malate-aspartate shuttle capacity declines rapidly after birth,
2) divergence of mitochondrial
malate dehydrogenase mRNA and protein levels during development
suggests posttranscriptional regulation of this protein, and
3) the developmental decline in
malate-aspartate shuttle capacity is regulated by decreased
oxoglutarate/malate carrier gene expression.
development; energy metabolism; gene expression; oxoglutarate/malate carrier; malate dehydrogenase
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