Grizzly bears, Ursus arctos horribilis, tolerate extended periods of extremely low heart rate during hibernation without developing congestive heart failure or chamber dilation. I hypothesized that relative MyHC isoform ratio would be unchanged during hibernation to maintain contractility during hibernation-associated bradycardia. Myosin heavy-chain (MyHC) proteins are the primary determinates of contractility, and I report a novel shift in expression toward MyHC-α isoform in the left atrium during hibernation. Interestingly, mRNA expression of atrogenes and their regulatory transcription factors is not increased in concert with ventricular atrophy, although myocardial IGF-I gene expression is decreased. Proteomic analysis of seasonal protein profiles from left atria and ventricles revealed no significant differences between groups. These findings highlight chamber-specific regulation of relative MyHC expression that may serve to optimize contractility during the altered hemodynamic state of hibernation, and suggest posttranscriptional regulation of cardiac atrophy in hibernating grizzly bears.
|Advisor:||Rourke, Bryan C.|
|School:||California State University, Long Beach|
|School Location:||United States -- California|
|Source:||MAI 49/05M, Masters Abstracts International|
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