Background: CNS lesions that are acquired early in life e.g. cerebral palsy (CP)
disturb muscle development and growth, while CNS injuries acquired later in
life e.g. stroke, affect fully matured muscles and cause paresis and atrophy. These differences may result in different contracture
phenotypes. Aim: The purpose of this study was to compare systemic
biomarkers and gene expression levels in muscle of individuals with CNS lesions
acquired early and later in life. Methods: Blood samples and muscle
biopsies were analyzed using Enzyme-linked immunosorbent assay and Real-time
PCR from n = 24 control participants, n = 14 individuals with cerebral palsy,
and n = 12 stroke survivors. Results:Systemicmarkers: Myostatin was significantly decreased in both the cerebral palsy (p = 0.0051), and the stroke group (p = 0.036). Creatine
Kinase-MB and C-Reactive Protein were significantly elevated in stroke patients
only (p < 0.007 & p > 0.034 respectively). Geneexpressions: The expression of myostatin (MSTN) was significantly lower in both the ST and
the CP group when compared to Ctrl (p = 0.02). In
addition, collagen type 4A1 (COL4A1) was significantly lower in the CP
group compared to the other groups (p = 0.015). Finally, the troponin 1 slow
skeletal muscle type was significantly increased in the ST group when compared
to both CP and Ctrl (p = 0.03). Conclusion: The downregulation of
myostatin in individuals with both early and late CNS injury is likely a
compensatory reaction to muscle weakness, reduced muscle mass and/or muscle atrophy. Changes in gene
expression may reflect a specific alteration depending on when in life the CNS lesions were acquired.
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