Abstract
The adenine nucleotide translocator or ADP/ATP carrier protein (AAC) is an integral protein present in the inner mitochondrial membrane, which performs the exchange of cytoplasmic and intramitochondrial ADP and ATP. The myocardial AAC content was studied in J-2-N cardiomyopathic hamsters. The AAC content was found to be significantly decreased in J-2-N hamsters. For molecular biological analysis, hamster AAC (T1 isoenzyme) cDNA was cloned by the plaque hybridization method. This AAC cDNA hybridized specifically with AAC mRNA, so RNA dot-blot hybridization was performed. The highest AAC mRNA level was observed in control hamsters followed by J-2-N hamsters with mild myocardial damage, J-2-N hamsters with severe myocardial damage and Bio 14-6 cardiomyopathic hamsters. These results suggest that a decreased AAC content may contribute to the pathogenesis of cardiomyopathy and that a decrease of AAC mRNA levels may explain the abnormalities of AAC in J-2-N cardiomyopathic hamsters.
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