4.4 Article

Gene and protein expression associated with protein synthesis and breakdown in paraplegic skeletal muscle

Journal

MUSCLE & NERVE
Volume 37, Issue 4, Pages 505-513

Publisher

WILEY
DOI: 10.1002/mus.20976

Keywords

chronic atrophy; FoxO; mTOR; MuRF1; spinal cord injury

Funding

  1. NHLBI NIH HHS [R01 HL074122-04, R01 HL 074122, R01 HL074122] Funding Source: Medline
  2. NIAMS NIH HHS [R01 AR049877, R01 AR 049877, R01 AR049877-05A1] Funding Source: Medline
  3. NIA NIH HHS [P30 AG024832] Funding Source: Medline
  4. NICHD NIH HHS [T32 HD007539, T32 HD007539-07] Funding Source: Medline

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Spinal cord injury reduces the rate of skeletal muscle protein synthesis and increases protein breakdown, resulting in rapid muscle loss. The purpose of this study was to determine whether long-term paraplegia would eventually result in a downregulation of muscle mRNA and protein expression associated with both protein synthesis and breakdown. After 10 weeks of spinal cord transection, soleus muscle from 12 rats (6 sham control, 6 paraplegic) was studied for mRNAs and proteins associated with protein synthesis and breakdown using real-time polymerase chain reaction and immunoblotting techniques. Protein kinase B (PKB/Akt), ribosomal S6 kinase 1 (S6K1), and myogenin mRNA were downregulated, whereas muscle ring finger 1 (MuRF1) and phospho-forkhead transcription factor 4 (FoxO4) protein were increased in paraplegic rats. We conclude that gene and protein expression of pathways associated with protein synthesis are reduced, whereas some markers of protein breakdown remain elevated following chronic paraplegia. Clinical interventions designed to increase muscle protein synthesis may be helpful in preventing excessive muscle loss during long-term paraplegia.

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