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Impact of metallothionein deficiency on soleus muscle function following acute spinal cord injury
Author(s) -
DeRuisseau Lara R,
Recca Daniel M,
Bidwell Amy J,
Orosz Nadia J,
Pompo Kimberly M,
DeRuisseau Keith C
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.962.25
Subject(s) - soleus muscle , metallothionein , muscle atrophy , spinal cord injury , spinal cord , skeletal muscle , atrophy , medicine , strain (injury) , hindlimb , endocrinology , chemistry , anesthesia , anatomy , biochemistry , gene , psychiatry
Metallothioneins (Mts) are small molecular weight proteins that possess metal binding and free radical scavenging properties. Furthermore, Mt is a stress protein that likely participates in the adaptive response of skeletal muscle to stressful stimuli and is up‐regulated following acute spinal cord injury (SCI). We tested the hypothesis that loss of Mt (Mt1 and Mt2; Mt −/ − ) would lead to exacerbated atrophy and contractile dysfunction of the soleus muscle following acute SCI (7 days, T9 transection) in Mt −/ − mice compared to control strain mice. Transected control strain (CT; n=5) and transected Mt −/ − (MT; n=6) mice experienced an equivalent % loss of body weight by day 7 of recovery compared to pre‐surgery weight (CT = −8.6 ± 1.6; MT = −11.6 ± 2.4). Soleus muscle mass (mg) of CT (4.3 ± 0.2) and MT (4.6 ± 0.1) groups was lower (p<0.05) than the non‐surgical control strain (NS; n=5; 5.6 ± 0.3). However, preliminary data (n=1–3/group) indicate that a lower maximal specific tension (N/cm 2 ) is generated by the soleus in MT vs. controls (NS=23.7 ± 2.5; CT=22.1; MT 19.0 ± 0.0). In summary, deficiency of Mt1 and Mt2 does not alter the loss of muscle mass but may lead to lower maximal force generating ability of the soleus in response to disuse resulting from spinal cord injury. Supported by Syracuse University SOE