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Gewählte Publikation:

Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2017

AutorInnen: Smorodchenko, A; Schneider, S; Rupprecht, A; Hilse, K; Sasgary, S; Zeitz, U; Erben, RG; Pohl, EE

Titel: UCP2 up-regulation within the course of autoimmune encephalomyelitis correlates with T-lymphocyte activation.

Quelle: Biochim Biophys Acta Mol Basis Dis. 2017; 1863(4):1002-1012

Autor/innen der Vetmeduni Vienna:

Erben Reinhold
Hilse-Koller Karolina
Pohl Elena
Rupprecht Anne
Sasgary Soleman
Schneider Stephanie
Smorodchenko Alina
Zeitz Ute

Beteiligte Vetmed-Organisationseinheiten
Institut für Physiologie, Pathophysiologie und Biophysik, Abteilung für Physiologie, Pathophysiologie und experimentelle Endokrinologie
Institut für Physiologie, Pathophysiologie und Biophysik, Abteilung für Physiologie und Biophysik

Multiple sclerosis (MS) is an inflammatory demyelinating autoimmune disorder of the central nervous system (CNS) associated with severe neurological disability. Reactive oxygen species (ROS) and mitochondrial dysfunction play a pivotal role in the pathogenesis of this disease. Several members of the mitochondrial uncoupling protein subfamily (UCP2-UCP5) were suggested to regulate ROS by diminishing the mitochondrial membrane potential and constitute therefore a promising pharmacological target for MS. To evaluate the role of different uncoupling proteins in neuroinflammation, we have investigated their expression patterns in murine brain and spinal cord (SC) during different stages of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. At mRNA and protein levels we found that only UCP2 is up-regulated in the SC, but not in brain. The increase in UCP2 expression was antigen-independent, reached its maximum between 14 and 21days in both OVA and MOG immunized animals and correlated with an augmented number of CD3+ T-lymphocytes in SC parenchyma. The decrease in abundance of UCP4 was due to neuronal injury and was only detected in CNS of MOG-induced EAE animals. The results provide evidence that the involvement of mitochondrial UCP2 in CNS inflammation during EAE may be mainly explained by the invasion of activated T-lymphocytes. This conclusion coincides with our previous observation that UCP2 is up-regulated in activated and rapidly proliferating T-cells and participates in fast metabolic re-programming of cells during proliferation.Copyright © 2017 Elsevier B.V. All rights reserved.

Keywords Pubmed: Animals
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimentalgeneticsimmunologypathology
Lymphocyte Activation
Mice, Inbred C57BL
Multiple Sclerosisgeneticsimmunologypathology
Spinal Cordimmunologymetabolismpathology
Uncoupling Protein 2geneticsimmunology

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