Submitted to: Physiological Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/27/2006
Publication Date: 12/1/2006
Citation: Salem, M., Kenney, B., Rexroad III, C.E., Yao, J. 2006. Microarray gene expression analysis in atrophying rainbow trout muscle: an unique non-mammalian muscle degradation model. Physiological Genomics 28:33-45.
Interpretive Summary: Muscle deterioration, or atrophy, can be caused by a variety of different physiological or pathological conditions. However, despite the diversity of signals the resulting biochemical changes in the deteriorating muscle share many common characteristics. In salmonids (trout and salmon) muscle deteriorates as a response to the needs of the fish for energy to fuel the spawning process which provides a unique model to investigate the mechanisms of muscle atrophy in non-mammalian vertebrates. In this study a microarray comprised of 16,006 cDNAs was used to investigate the expression of genes in the fast switch muscle of gravid females compared to sterile fish. A total of 202 genes were reproducibly identified as differing in the reproductive vs sterile fish. The results suggested that, for the most part, the changes occurring during muscle atrophy in fish are similar to those occurring in mammals. However, some changes unique to the fish model and the presence of genes shown for the first time to be associated with muscle atrophy warrant further investigations.
Technical Abstract: Muscle atrophy is a physiological response to diverse physiological and pathological conditions that trigger muscle deterioration through distinct cellular stimuli. Despite different physiological signals, the resulting biochemical changes in atrophying muscle share many common cascades. Muscle deterioration as a physiological response to the energetic demands of fish spawning represents a unique model for studying the mechanisms of muscle degradation in non-mammalian animals. A salmonid microarray, containing 16,006 cDNAs, was used to study the transcriptome response to atrophying fast-switch muscles from gravid rainbow trout in comparison to sterile fish. A total of 202 unique transcripts were reproducibly identified as 82 up- and 120 down-regulated genes in atrophying muscles. Transcripts having gene ontology biological process identifiers were grouped according to their functions. Muscle deterioration was associated with elevated expression of genes involved in the catheptic and collagenase proteolytic pathways, the aerobic ATP production, buffering, utilization and growth arrest. Whereas, atrophying muscle showed down-regulation of genes encoding serpin (a serine proteinase inhibitor), enzymes of anaerobic respiration, muscle proteins as well as genes required for RNA and protein biosynthesis/processing. Therefore, gene transcription of atrophying trout muscle changed in a manner similar to mammalian muscle atrophy. These changes result in an arrest of normal cell growth, net protein loss, and a decreased dependence on glycolytic cellular respiration characteristic of fast-switch muscle to aerobic respiratory mechanisms. Other changes/mechanisms unique to the fish model were discussed including genes associated with muscle atrophy reported for the first time.