@article{2999332,
    title = "Alternations of 14-3-3 θ and β protein levels in brain during experimental sepsis",
    author = "Memos, N. and Kataki, A. and Chatziganni, E. and Nikolopoulou, M. and Skoulakis, E. and Consoulas, C. and Zografos, G. and Konstadoulakis, M.",
    journal = "Journal of Neuroscience Research",
    year = "2011",
    volume = "89",
    number = "9",
    pages = "1409-1418",
    issn = "0360-4012, 1097-4547",
    doi = "10.1002/jnr.22673",
    keywords = "brain protein;  glial fibrillary acidic protein;  mitogen activated protein kinase p38;  neuron specific nuclear protein;  phosphoprotein;  protein 14 3 3;  protein 14 3 3 beta;  protein 14 3 3 theta;  unclassified drug, animal cell;  animal experiment;  animal model;  animal tissue;  apoptosis;  article;  astrocyte;  brain nerve cell;  controlled study;  down regulation;  experimental infection;  hippocampus;  immunohistochemistry;  male;  nerve cell necrosis;  nonhuman;  priority journal;  protein expression;  protein localization;  Purkinje cell;  rat;  sepsis;  time, 14-3-3 Proteins;  Animals;  Apoptosis;  Brain;  Cecum;  Disease Models, Animal;  Male;  Neurons;  Protein Isoforms;  Rats;  Rats, Wistar;  Sepsis;  Time Factors;  Tissue Distribution",
    abstract = "The 14-3-3 family members play a crucial role in the determination of cell fate, exerting their antiapoptotic activity through directly interfering with the critical function of the mitochondrial core proapoptotic machinery. Dimerization of 14-3-3 is vital for the interaction with many of its client proteins and is regulated by phosphorylation. In a previous study, we observed time-dependent neuronal apoptosis during sepsis. Therefore, in the present study, we sought to evaluate the expression of 14-3-3 θ and β isoforms in septic brain and their association with apoptosis. Sepsis was induced by a CLP model in Wistar rats that were sacrificed at predefined time points. Flow cytometric analysis showed a sepsis-induced, time-dependent alteration of 14-3-3 θ and β isoforms in both Neun + and GFAP + cells. 14-3-3 θ was linearly correlated with apoptosis, and stratified analysis for alive and apoptotic neuronal cells demonstrated a gradual down-regulation of θ isoform in alive neurons and astrocytes. The phospho-P38 (pP38) MAP kinase levels were altered in a time-dependent manner during sepsis, presenting a peak at 6 hr post-CLP. A significant correlation between the two isoforms of 14-3-3 was observed in septic rats, with the θ isoform predominant at all time points. The hippocampus, Purkinje cells, and glia-like cells showed intense immunohistochemical reactivity for 14-3-3 θ isoform, whereas the choroid plexus showed constantly increased β isoform expression. Our results showed that sepsis alters the expression of both 14-3-3 θ and β isoforms in a time-, cell-, and topography-dependent manner. © 2011 Wiley-Liss, Inc."
}