TY - JOUR
T1 - Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection
AU - Wu, Yong
AU - Collier, Lauren
AU - Qin, Weiping
AU - Creasey, Graham
AU - Bauman, William A.
AU - Jarvis, Jonathan
AU - Cardozo, Christopher
N1 - Funding Information:
This work was supported by the Veterans Health Administration, Rehabilitation Research and Development Service (grants B9212C to WAB and B4055X and B3347K to CC) and European Commission Project RISE QLG5-CT-2001-02191 to JCJ. We wish to thank Drs. Hunter Peckham from the Cleveland FES Center and Ron Triolo from and Advanced Platforms Technology Center, both of which are Centers of Excellence of the Rehabilitation R&D Service of the US Department of Veterans Affairs, for many helpful discussions during the design of these experiments. We also wish to thank Yuzhong Wu for sketching the animal model.
PY - 2013
Y1 - 2013
N2 - BACKGROUND: Spinal cord injury (SCI) results in muscle atrophy and a shift of slow oxidative to fast glycolytic fibers. Electrical stimulation (ES) at least partially restores muscle mass and fiber type distribution. The objective of this study was to was to characterize the early molecular adaptations that occur in rat soleus muscle after initiating isometric resistance exercise by ES for one hour per day for 1, 3 or 7 days when ES was begun 16 weeks after SCI. Additionally, changes in mRNA levels after ES were compared with those induced in soleus at the same time points after gastrocnemius tenotomy (GA).RESULTS: ES increased expression of Hey1 and Pitx2 suggesting increased Notch and Wnt signaling, respectively, but did not normalize RCAN1.4, a measure of calcineurin/NFAT signaling, or PGC-1ß mRNA levels. ES increased PGC-1α expression but not that of slow myofibrillar genes. Microarray analysis showed that after ES, genes coding for calcium binding proteins and nicotinic acetylcholine receptors were increased, and the expression of genes involved in blood vessel formation and morphogenesis was altered. Of the 165 genes altered by ES only 16 were also differentially expressed after GA, of which 12 were altered in the same direction by ES and GA. In contrast to ES, GA induced expression of genes related to oxidative phosphorylation.CONCLUSIONS: Notch and Wnt signaling may be involved in ES-induced increases in the mass of paralyzed muscle. Molecular adaptations of paralyzed soleus to resistance exercise are delayed or defective compared to normally innervated muscle.
AB - BACKGROUND: Spinal cord injury (SCI) results in muscle atrophy and a shift of slow oxidative to fast glycolytic fibers. Electrical stimulation (ES) at least partially restores muscle mass and fiber type distribution. The objective of this study was to was to characterize the early molecular adaptations that occur in rat soleus muscle after initiating isometric resistance exercise by ES for one hour per day for 1, 3 or 7 days when ES was begun 16 weeks after SCI. Additionally, changes in mRNA levels after ES were compared with those induced in soleus at the same time points after gastrocnemius tenotomy (GA).RESULTS: ES increased expression of Hey1 and Pitx2 suggesting increased Notch and Wnt signaling, respectively, but did not normalize RCAN1.4, a measure of calcineurin/NFAT signaling, or PGC-1ß mRNA levels. ES increased PGC-1α expression but not that of slow myofibrillar genes. Microarray analysis showed that after ES, genes coding for calcium binding proteins and nicotinic acetylcholine receptors were increased, and the expression of genes involved in blood vessel formation and morphogenesis was altered. Of the 165 genes altered by ES only 16 were also differentially expressed after GA, of which 12 were altered in the same direction by ES and GA. In contrast to ES, GA induced expression of genes related to oxidative phosphorylation.CONCLUSIONS: Notch and Wnt signaling may be involved in ES-induced increases in the mass of paralyzed muscle. Molecular adaptations of paralyzed soleus to resistance exercise are delayed or defective compared to normally innervated muscle.
UR - http://www.scopus.com/inward/record.url?scp=84880994455&partnerID=8YFLogxK
U2 - 10.1186/1471-2202-14-81
DO - 10.1186/1471-2202-14-81
M3 - Article
C2 - 23914941
AN - SCOPUS:84880994455
SN - 1471-2202
VL - 14
SP - 81
JO - BMC Neuroscience
JF - BMC Neuroscience
ER -