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Sepsis-Induced Channelopathy in Skeletal Muscles is Associated with Expression of Non-Selective Channels.
Balboa, Elisa; Saavedra-Leiva, Fujiko; Cea, Luis A; Vargas, Aníbal A; Ramírez, Valeria; Escamilla, Rosalba; Sáez, Juan C; Regueira, Tomás.
Afiliación
  • Balboa E; Departamento de Fisiología, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • Saavedra-Leiva F; Centro de pacientes críticos, Clínica las Condes, Santiago, Chile.
  • Cea LA; Departamento de Fisiología, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • Vargas AA; Centro de pacientes críticos, Clínica las Condes, Santiago, Chile.
  • Ramírez V; Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
  • Escamilla R; Departamento de Fisiología, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • Sáez JC; Centro de pacientes críticos, Clínica las Condes, Santiago, Chile.
  • Regueira T; Departamento de Fisiología, Pontificia Universidad Católica de Chile, Santiago, Chile.
Shock ; 49(2): 221-228, 2018 02.
Article en En | MEDLINE | ID: mdl-28562477
Skeletal muscles (∼50% of the body weight) are affected during acute and late sepsis and represent one sepsis associate organ dysfunction. Cell membrane changes have been proposed to result from a channelopathy of yet unknown cause associated with mitochondrial dysfunction and muscle atrophy. We hypothesize that the channelopathy might be explained at least in part by the expression of non-selective channels. Here, this possibility was studied in a characterized mice model of late sepsis with evident skeletal muscle atrophy induced by cecal ligation and puncture (CLP). At day seven after CLP, skeletal myofibers were found to present de novo expression (immunofluorescence) of connexins 39, 43, and 45 and P2X7 receptor whereas pannexin1 did not show significant changes. These changes were associated with increased sarcolemma permeability (∼4 fold higher dye uptake assay), ∼25% elevated in intracellular free-Ca concentration (FURA-2), activation of protein degradation via ubiquitin proteasome pathway (Murf and Atrogin 1 reactivity), moderate reduction in oxygen consumption not explained by changes in levels of relevant respiratory proteins, ∼3 fold decreased mitochondrial membrane potential (MitoTracker Red CMXRos) and ∼4 fold increased mitochondrial superoxide production (MitoSox). Since connexin hemichannels and P2X7 receptors are permeable to ions and small molecules, it is likely that they are main protagonists in the channelopathy by reducing the electrochemical gradient across the cell membrane resulting in detrimental metabolic changes and muscular atrophy.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Atrofia Muscular / Músculo Esquelético / Canalopatías Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Shock Asunto de la revista: ANGIOLOGIA / CARDIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Chile

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Atrofia Muscular / Músculo Esquelético / Canalopatías Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Shock Asunto de la revista: ANGIOLOGIA / CARDIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Chile