Journal:American Journal of Physiology. Endocrinology and Metabolism
Year, Volume, Issue, Page(s):16, 310, 9, E754-E761
Study assessed the effects of gene expression or intracellular signaling in paralyzed muscles of men with long-standing spinal cord injury (SCI). Specifically, it examined the expression of genes (TNFαR, TNFα, IL-6R, IL-6, TWEAK, TWEAK R, atrogin-1, and MuRF1) and abundance of intracellular signaling proteins (TWEAK, TWEAK R, NF-κB, and p-p65/p-50/105) that are known to mediate inflammation and atrophy in skeletal muscle. For further insight into the distribution and variability of muscle fiber size, researchers also analyzed the frequency distribution of SCI fiber size. Resting vastus lateralis (VL) muscle biopsy samples were taken from 11 men with long-standing SCI and compared with VL samples from 11 able-bodied men of similar age. ккIn addition, based on the effects of muscle inflammation on promotion of skeletal muscle fibrosis, they assessed the degree of fibrosis between myofibers and fascicles in both groups. Results demonstrated that chronic SCI muscle has heightened TNFαR and TWEAK R gene expression and NF-κB signaling (higher TWEAK R and phospho-NF-κB p65) and fibrosis, along with substantial myofiber size heterogeneity, compared with able-bodied individuals. These data suggest that the TWEAK/TWEAK R/NF-κB signaling pathway may be an important mediator of chronic inflammation and fibrotic adaptation in SCI muscle.