Altered autophagy gene expression and persistent atrophy suggest impaired remodeling in chronic hemiplegic human skeletal muscle

Ferdinand von Walden, Finnbogi Jakobsson, Lars Edström, Gustavo Alberto Nader

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Introduction:: Upper motor neuron lesions after stroke are a major cause of disability. We aimed to determine whether skeletal muscles from these patients display typical molecular signatures of inflammation, growth arrest, and atrophy. Methods:: Muscle biopsies were analyzed for morphological, histochemical, ultrastructural, and molecular features indicative of changes in gene expression involved in muscle atrophy. Results:: Chronic hemiplegia resulted in {reversed tilde}9.5% atrophy, fiber type shifts, and histochemical and ultrastructural signs of impaired remodeling. TNF and TWEAK expressions were unaltered, but MSTN mRNA was lower (-73%, P < 0.05) in paretic tibialis anterior vs. age-matched controls. The expression of autophagy-related genes (BCN-1, LC3, and GABARAPL1) was lower in paretic tibialis anterior (-81%, -48%, and -60%, respectively, P < 0.01) and soleus (-85%, -54%, and -60% respectively, P < 0.01) compared with old controls. Conclusions:: Persistent atrophy in chronic spastic hemiplegia may be associated with impaired remodeling partly due to altered autophagy gene expression.

Original languageEnglish (US)
Pages (from-to)785-792
Number of pages8
JournalMuscle and Nerve
Volume46
Issue number5
DOIs
StatePublished - Nov 2012

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Physiology (medical)
  • Physiology

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