Altered oxidative stress and antioxidant defence in skeletal muscle during the first year following spinal cord injury.

Oxidative stress promotes protein degradation and apoptosis in skeletal muscle undergoing atrophy. We aimed to determine whether spinal cord injury leads to changes in oxidative stress, antioxidant capacity, and apoptotic signaling in human skeletal muscle during the first year after spinal cord injury. Vastus lateralis biopsies were obtained from seven individuals 1, 3, and 12 months after spinal cord injury and from seven able-bodied controls.

Retained differentiation capacity of human skeletal muscle satellite cells from spinal cord-injured individuals.

Despite the well-known role of satellite cells in skeletal muscle plasticity, the effect of spinal cord injury on their function in humans remains unknown. We determined whether spinal cord injury affects the intrinsic ability of satellite cells to differentiate and produce metabolically healthy myotubes. We obtained vastus lateralis biopsies from eight spinal cord-injured and six able-bodied individuals.

Protein translation, proteolysis and autophagy in human skeletal muscle atrophy after spinal cord injury.

Aim: Spinal cord injury-induced loss of skeletal muscle mass does not progress linearly. In humans, peak muscle loss occurs during the first 6 weeks postinjury, and gradually continues thereafter. The aim of this study was to delineate the regulatory events underlying skeletal muscle atrophy during the first year following spinal cord injury.

MicroRNA-208b progressively declines after spinal cord injury in humans and is inversely related to myostatin expression.

The effects of long-term physical inactivity on the expression of microRNAs involved in the regulation of skeletal muscle mass in humans are largely unknown. MicroRNAs are short, noncoding RNAs that fine-tune target expression through mRNA degradation or by inhibiting protein translation. Intronic to the slow, type I, muscle fiber type genes MYH7 and MYH7b, microRNA-208b and microRNA-499-5p are thought to fine-tune the expression of genes important for muscle growth, such as myostatin.

Altered content of AMP-activated protein kinase isoforms in skeletal muscle from spinal cord injured subjects.

AMP-activated protein kinase (AMPK) is a pivotal regulator of energy homeostasis. Although downstream targets of AMPK are widely characterized, the physiological factors governing isoform expression of this protein kinase are largely unknown. Nerve/contractile activity has a major impact on the metabolic phenotype of skeletal muscle, therefore likely to influence AMPK isoform expression.