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  • Influence of chronic and acute spinal cord injury on skeletal muscle Na+/K+-ATPase and phospholemman expression in humans
    Boon, Hanneke ...
    Na(+)/K(+)-ATPase is an integral membrane protein crucial for the maintenance of ion homeostasis and skeletal muscle contractibility. Skeletal muscle Na(+)/K(+)-ATPase content displays remarkable ... plasticity in response to long-term increase in physiological demand, such as exercise training. However, the adaptations in Na(+)/K(+)-ATPase function in response to a suddenly decreased and/or habitually low level of physical activity, especially after a spinal cord injury (SCI), is incompletely known. We testedthe hypothesis that skeletal muscle content of Na(+)/K(+)-ATPase and theassociated regulatory proteins from the FXYD family, is altered in SCI patients in a manner dependent on the severity of the spinal cord lesion and post-injury level of physical activity. Three different groups were studied: (i) six subjects with chronic complete cervical SCI (ii) seven subjects with acute, complete cervical SCI and (iii) six subjects with acute, incomplete cervical SCI. The individuals in groups (ii) and (iii) were studied at month 1, 3 and 12 post-injury, whereas individuals with chronic SCI were compared toan able-bodied control group. Chronic complete SCI was associated with a marked decrease in š(3)Hđouabain binding site concentration in skeletal muscle as well as reduced protein content of the alpha1, alpha2 and beta1 subunit of the Na(+)/K(+)-ATPase. In line with this finding, expression of Na(+)/K(+)-ATPase alpha1 and alpha2 subunits progressively decreased during the first year after complete, but not after incomplete SCI. The expression ofthe regulatory protein phospholemman (PLM or FXYD1) was attenuated after complete, but not incomplete, cervical SCI. In contrast, FXYD5 was substantially up-regulated in patients with complete SCI. (Abs. trunc. at 2000ch.)
    Vrsta gradiva - članek, sestavni del
    Leto - 2012
    Jezik - angleški
    COBISS.SI-ID - 29450969
    DOI