title: Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection.
abstract: 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.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wu
authors.forename: Lauren
authors.initials: L
authors.lastname: Collier
authors.forename: Weiping
authors.initials: W
authors.lastname: Qin
authors.forename: Graham
authors.initials: G
authors.lastname: Creasey
authors.forename: William A
authors.initials: WA
authors.lastname: Bauman
authors.forename: Jonathan
authors.initials: J
authors.lastname: Jarvis
authors.forename: Christopher
authors.initials: C
authors.lastname: Cardozo
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D004599:Electric Stimulation Therapy; D005260:Female; D005786:Gene Expression Regulation; D018398:Homeodomain Proteins / Q000378:metabolism; D009045:Motor Endplate / Q000235:genetics*; D018482:Muscle, Skeletal / Q000378:metabolism*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D051381:Rats; D017208:Rats, Wistar; D012097:Repressor Proteins / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000235:genetics* / Q000628:therapy*; D014157:Transcription Factors / Q000378:metabolism; D060449:Wnt Signaling Pathway; D000097577:Homeobox Protein PITX2
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D002118:Calcium; D018398:Homeodomain Proteins; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012097:Repressor Proteins; D014157:Transcription Factors; D000097577:Homeobox Protein PITX2; C405694:Hairy, HRT1 protein; C501429:Ppargc1a protein, rat
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