NERVE-RESPONSIVE TROPONIN-I SLOW PROMOTER DOES NOT RESPOND TO UNLOADING

We examined the regulation of the troponin I slow (TnIs) promoter duri ng skeletal muscle unloading-induced protein isoform transition, by us ing a transgenic mouse line harboring the -4,200 to +12 base pairs reg ion of the human TnIs promoter. Eighteen female transgenic mice (-30 g body mass) were randomly divided into two groups: weight-bearing (WE) controls (n = 9) and hindIimb unloaded (HU; It = 9). The HU mice were tail suspended for 7 days. Body mass was unchanged in the WE group bu t was reduced (-6%; P < 0.05) after the HU treatment. Absolute soleus muscle mass (-25%) and soleus mass relative to body mass (-16%) were b oth lower (P < 0.05) in the HU group compared with the WB mice. Northe rn blot analyses indicate that 7 days of HU result in a 64% decrease ( P < 0.05) in the abundance of endogenous TnIs mRNA (mu g/mg muscle) in the mouse soleus. Furthermore, there is a trend for the abundance of the fast troponin I mRNA to be increased (+34%). Analysis of transgeni c chloramphenicol acetyltransferase activity in the soleus muscle reve aled no difference (P > 0.05) between WE and HU groups. We conclude th at additional elements are necessary for the TnIs gene to respond to a n unloading-induced, slow-to-fast isoform transition stimulus.