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Articles in PresS, published online ahead of print September 17, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00294.2002
Submitted on July 8, 2002
Accepted on September 4, 2002
1 Department of Kinesiology and Health Science, York University, Toronto, Ont, Canada
2 Department of Pathology, Northwestern University, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: dhood{at}yorku.ca.
Thyroid hormone (T3) induces phenotypic alterations in cardiac mitochondria, in part by influencing protein import and the expression of the import motor mtHsp70. Here, we examined the adaptability of translocases of the inner membrane (Tim) proteins, as well as the outer membrane receptor Tom34, in response to T3. Administration of T3 to rats for 5 days increased cardiac Tim23 and Tim44 mRNA levels by 55% and 50%, respectively, but had no effect on Tim17. T3 treatment also induced a 45% increase in Tom34 mRNA, with no accompanying changes at the protein level, suggesting regulation at the post-transcriptional level. In H9c2 cardiac cells, Tim17 mRNA was elevated by 114% by 9 days of differentiation, while Tim23 and Tim44 declined by 25% and 29%, respectively. To determine the functional consequences of these T3-induced changes, MDH import rates were measured in H9c2 cells stably overexpressing Tim44 and mtHsp70, either alone or in combination. MDH import remained unaltered in cells overexpressing Tim44, or in cells overexpressing both Tim44 and mtHsp70. However, when mtHsp70 was overexpressed alone, a 13% (p<0.05) increase in MDH import rate was observed. These findings indicate that import machinery components are differentially regulated in response to stimuli which induce mitochondrial biogenesis, like T3 and differentiation. In addition, the induction of an import machinery component in response to T3 may not necessarily result in functional changes in protein import during mitochondrial biogenesis. Finally, mHsp70 may play a regulatory role in the import process which is independent of its interaction with Tim44.
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