Nerve-responsive troponin I slow promoter does not respond to unloading

We examined theregulation of the troponin I slow (TnIs) promoter during skeletalmuscle unloading-induced protein isoform transition, by using atransgenic mouse line harboring the 4,200 to +12 base pairsregion of the human TnIs promoter. Eighteen female transgenic mice(~30 g body mass) were randomly divided into two groups:weight-bearing (WB) controls (n = 9)and hindlimb unloaded (HU; n = 9). TheHU mice were tail suspended for 7 days. Body mass was unchanged in theWB group but was reduced (6%; P < 0.05) after the HU treatment.Absolute soleus muscle mass (25%) and soleus mass relative tobody mass (16%) were both lower(P < 0.05) in the HU group comparedwith the WB mice. Northern blot analyses indicate that 7 days of HUresult in a 64% decrease (P < 0.05)in the abundance of endogenous TnIs mRNA (µg/mg muscle) in the mousesoleus. Furthermore, there is a trend for the abundance of the fasttroponin I mRNA to be increased (+34%). Analysis of transgenicchloramphenicol acetyltransferase activity in the soleus musclerevealed no difference (P > 0.05)between WB and HU groups. We conclude that additional elements arenecessary for the TnIs gene to respond to an unloading-induced,slow-to-fast isoform transition stimulus.