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Nerve-responsive troponin I slow promoter does not respond to unloadingWe examined the regulation of the troponin I slow (TnIs) promoter during skeletal muscle unloading-induced protein isoform transition, by using a transgenic mouse line harboring the -4,200 to +12 base pairs region of the human TnIs promoter. Eighteen female transgenic mice ( approximately 30 g body mass) were randomly divided into two groups: weight-bearing (WB) controls (n = 9) and hindlimb unloaded (HU; n = 9). The HU mice were tail suspended for 7 days. Body mass was unchanged in the WB group but was reduced (-6%; P < 0.05) after 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 with the WB mice. Northern blot analyses indicate that 7 days of HU result in a 64% decrease (P < 0.05) in the abundance of endogenous TnIs mRNA (microg/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 transgenic chloramphenicol acetyltransferase 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.
Document ID
20040172734
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Criswell, D. S.
(University of Texas Medical School Houston, Texas 77030, United States)
Hodgson, V. R.
Hardeman, E. C.
Booth, F. W.
Date Acquired
August 22, 2013
Publication Date
March 1, 1998
Publication Information
Publication: Journal of applied physiology (Bethesda, Md. : 1985)
Volume: 84
Issue: 3
ISSN: 8750-7587
Subject Category
Aerospace Medicine
Distribution Limits
Public
Copyright
Other
Keywords
Non-NASA Center
NASA Discipline Musculoskeletal

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