<strong>Background:</strong><span><span><span style="font-family:;" "=""> CNS lesions that are acquired early in life e.g. cerebral palsy (CP) disturb muscle deve...<strong>Background:</strong><span><span><span style="font-family:;" "=""> 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</span></span></span><span><span><span style="font-family:;" "="">,</span></span></span><span><span><span style="font-family:;" "=""> affect fully matured muscles and <span>cause</span> paresis and atrophy. These differences may result in different contracture phenotypes. <b>Aim:</b> 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. <b>Methods:</b> 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. <b>Results:</b> <b>Systemic</b> <b>markers:</b> Myostatin was significantly decreased in both the cerebral palsy (p = 0.0051<span>),</span> 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). <b>Gene</b> <b>expressions:</b> The expression of myostatin (MSTN) was significantly lower in both the ST and the CP group when compared to Ctrl (p = 0.02). <span>In addition</span>, 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). <b>Conclusion:</b> The downregulation of myostatin in individuals with both early and late CNS injury is likely a compensatory reaction to muscle weakness, reduced muscle mass <span>and</span>/or muscle atrophy. Changes in gene expression may reflect <span>a specific</span> alteration depending on when in life the CNS lesions were acquired.</span></span></span>展开更多
文摘<strong>Background:</strong><span><span><span style="font-family:;" "=""> 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</span></span></span><span><span><span style="font-family:;" "="">,</span></span></span><span><span><span style="font-family:;" "=""> affect fully matured muscles and <span>cause</span> paresis and atrophy. These differences may result in different contracture phenotypes. <b>Aim:</b> 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. <b>Methods:</b> 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. <b>Results:</b> <b>Systemic</b> <b>markers:</b> Myostatin was significantly decreased in both the cerebral palsy (p = 0.0051<span>),</span> 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). <b>Gene</b> <b>expressions:</b> The expression of myostatin (MSTN) was significantly lower in both the ST and the CP group when compared to Ctrl (p = 0.02). <span>In addition</span>, 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). <b>Conclusion:</b> The downregulation of myostatin in individuals with both early and late CNS injury is likely a compensatory reaction to muscle weakness, reduced muscle mass <span>and</span>/or muscle atrophy. Changes in gene expression may reflect <span>a specific</span> alteration depending on when in life the CNS lesions were acquired.</span></span></span>
