Exercise-induced gene expression in soleus muscle is dependent on time after spinal cord injury in rats.
Cycling exercise attenuates atrophy in hindlimb muscles and causes changes in spinal cord properties after spinal cord injury in rats. We hypothesized that exercising soleus muscle expresses genes that are potentially beneficial to the injured spinal cord. Rats underwent spinal cord injury at T10 and were exercised on a motor-driven bicycle. Soleus muscle and lumbar spinal cord tissue were used for messenger RNA (mRNA) analysis. Gene expression of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) was elevated 11- and 14-fold, respectively, in soleus muscle after one bout of exercise performed 5 days after spinal cord transection. Also, c-fos and heat shock protein-27 (HSP27) mRNA abundance were increased 11- and 7-fold, respectively. When exercise was started 2 days after the injury, the changes in gene expression were not observed. By contrast, at 2 but not at 5 days after transection, expression of the HSP27 gene was elevated sixfold in the lumbar spinal cord, independent of exercise. Electromyographic activity in soleus muscles was also decreased at 2 days, indicating that the spinal cord was less permissive to exercise at this early time. Long-term exercise for 4 weeks attenuated muscle atrophy equally well in rats started at 2 days or 5 days after injury. We conclude that BDNF and GDNF released from exercising muscle may be involved in exercise-induced plasticity of the spinal cord. Furthermore, the data suggest that the lumbar spinal cord undergoes time-dependent changes that temporarily impede the ability of the muscle to respond to exercise.
Dupont-Versteegden
Esther E
EE
Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, Arkansas 72205, USA. duponttesthere@uams.edu
Houlé
John D
JD
Dennis
Richard A
RA
Zhang
Junming
J
Knox
Micheal
M
Wagoner
Gail
G
Peterson
Charlotte A
CA
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics; D005260:Female; D051100:Glial Cell Line-Derived Neurotrophic Factor; D055551:HSP27 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D018482:Muscle, Skeletal / Q000294:innervation / Q000378:metabolism* / Q000503:physiopathology; D009133:Muscular Atrophy / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D009363:Neoplasm Proteins / Q000235:genetics; D009414:Nerve Growth Factors / Q000235:genetics*; D009473:Neuronal Plasticity / Q000235:genetics; D010805:Physical Conditioning, Animal; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000235:genetics; D013116:Spinal Cord / Q000378:metabolism / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000150:complications*; D013997:Time Factors; D015854:Up-Regulation / Q000235:genetics
D019208:Brain-Derived Neurotrophic Factor; C495041:Gdnf protein, rat; D051100:Glial Cell Line-Derived Neurotrophic Factor; D055551:HSP27 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C486114:Hspb1 protein, rat; D009363:Neoplasm Proteins; D009414:Nerve Growth Factors; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger