Abstract
810 We have examined the regulation of the Troponin I slow (TnIs) promoter during skeletal muscle unloading-induced protein isoform transition, using a transgenic mouse line harboring the -4200 to +12 bp region of the human TnIs promoter. Eighteen female transgenic mice (≈30 g body mass) were randomly divided into two groups: 1) weight-bearing (WB) controls, n=9, and 2) hindlimb unloaded (HU), n=9. The HU group were tail suspended for seven days. Body mass was unchanged in the WB group, but was reduced (-6%; P<0.05) following the HU treatment. Absolute soleus muscle mass (-25%) and soleus mass relative to body mass (-16%) were both lower (P<0.05) in the HU group compared to the WB mice. Northern blot analyses indicate that 7 days of HU results in a 64% decrease (P<0.05) in the abundance of endogenous TnIs mRNA (μg/mg muscle) in the mouse soleus. Further, there is a trend for the abundance of the fast TnI mRNA to be increased (+34%). Analysis of transgenic CAT activity in the soleus muscle revealed no difference (P>0.05) between WB and HU groups. We conclude that additional elements are necessary for the TnIs gene to respond to an unloading-induced slow-to-fast isoform transition stimulus.
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