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A selenoprotein T-derived peptide protects the heart against ischaemia/reperfusion injury through inhibition of apoptosis and oxidative stress.
Rocca, C; Boukhzar, L; Granieri, M C; Alsharif, I; Mazza, R; Lefranc, B; Tota, B; Leprince, J; Cerra, M C; Anouar, Y; Angelone, T.
Afiliación
  • Rocca C; Laboratory of Cellular and Molecular Cardiovascular Physiology, Department of Biology, Ecology and E.S., University of Calabria, Rende, Italy.
  • Boukhzar L; Laboratoire de Différenciation et Communication Neuronale et Neuroendocrine, Institut de Recherche et d'Innovation Biomédicale de Normandie and Centre Universitaire de Recherche et D'Innovation en Biologie, Normandie University, UNIROUEN, INSERM, Rouen, France.
  • Granieri MC; Laboratoire de Différenciation et Communication Neuronale et Neuroendocrine, Institut de Recherche et d'Innovation Biomédicale de Normandie and Centre Universitaire de Recherche et D'Innovation en Biologie, Normandie University, UNIROUEN, INSERM, Rouen, France.
  • Alsharif I; Laboratory of Cellular and Molecular Cardiovascular Physiology, Department of Biology, Ecology and E.S., University of Calabria, Rende, Italy.
  • Mazza R; Laboratoire de Différenciation et Communication Neuronale et Neuroendocrine, Institut de Recherche et d'Innovation Biomédicale de Normandie and Centre Universitaire de Recherche et D'Innovation en Biologie, Normandie University, UNIROUEN, INSERM, Rouen, France.
  • Lefranc B; Laboratory of Cellular and Molecular Cardiovascular Physiology, Department of Biology, Ecology and E.S., University of Calabria, Rende, Italy.
  • Tota B; Laboratoire de Différenciation et Communication Neuronale et Neuroendocrine, Institut de Recherche et d'Innovation Biomédicale de Normandie and Centre Universitaire de Recherche et D'Innovation en Biologie, Normandie University, UNIROUEN, INSERM, Rouen, France.
  • Leprince J; Laboratory of Cellular and Molecular Cardiovascular Physiology, Department of Biology, Ecology and E.S., University of Calabria, Rende, Italy.
  • Cerra MC; National Institute of Cardiovascular Research (INRC), Bologna, Italy.
  • Anouar Y; Laboratoire de Différenciation et Communication Neuronale et Neuroendocrine, Institut de Recherche et d'Innovation Biomédicale de Normandie and Centre Universitaire de Recherche et D'Innovation en Biologie, Normandie University, UNIROUEN, INSERM, Rouen, France.
  • Angelone T; Laboratory of Cellular and Molecular Cardiovascular Physiology, Department of Biology, Ecology and E.S., University of Calabria, Rende, Italy.
Acta Physiol (Oxf) ; 223(4): e13067, 2018 08.
Article en En | MEDLINE | ID: mdl-29575758
AIM: Selenoprotein T (SelT or SELENOT) is a novel thioredoxin-like enzyme whose genetic ablation in mice results in early embryonic lethality. SelT exerts an essential cytoprotective action during development and after injury through its redox-active catalytic site. This study aimed to determine the expression and regulation of SelT in the mammalian heart in normal and pathological conditions and to evaluate the cardioprotective effect of a SelT-derived peptide, SelT43-52(PSELT) encompassing the redox motif which is key to its function, against ischaemia/reperfusion(I/R) injury. METHODS: We used the isolated Langendorff rat heart model and different analyses by immunohistochemistry, Western blot and ELISA. RESULTS: We found that SelT expression is very abundant in embryo but is undetectable in adult heart. However, SelT expression was tremendously increased after I/R. PSELT (5 nmol/L) was able to induce pharmacological post-conditioning cardioprotection as evidenced by a significant recovery of contractility (dLVP) and reduction of infarct size (IS), without changes in cardiac contracture (LVEDP). In contrast, a control peptide lacking the redox site did not confer cardioprotection. Immunoblot analysis showed that PSELT-dependent cardioprotection is accompanied by a significant increase in phosphorylated Akt, Erk-1/2 and Gsk3α-ß, and a decrement of p38MAPK. PSELT inhibited the pro-apoptotic factors Bax, caspase 3 and cytochrome c and stimulated the anti-apoptotic factor Bcl-2. Furthermore, PSELT significantly reduced several markers of I/R-induced oxidative and nitrosative stress. CONCLUSION: These results unravel the role of SelT as a cardiac modulator and identify PSELT as an effective pharmacological post-conditioning agent able to protect the heart after ischaemic injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fragmentos de Péptidos / Reductasa de Tiorredoxina-Disulfuro / Daño por Reperfusión Miocárdica / Apoptosis / Estrés Oxidativo / Miocitos Cardíacos / Selenoproteínas / Infarto del Miocardio / Antioxidantes Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Acta Physiol (Oxf) Asunto de la revista: FISIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fragmentos de Péptidos / Reductasa de Tiorredoxina-Disulfuro / Daño por Reperfusión Miocárdica / Apoptosis / Estrés Oxidativo / Miocitos Cardíacos / Selenoproteínas / Infarto del Miocardio / Antioxidantes Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Acta Physiol (Oxf) Asunto de la revista: FISIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Reino Unido