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Evaluation of the fibroblast growth factor receptor 1 (FGFR1) in experimental autoimmune encephalomyelitis (EAE)

Bewertung des Fibroblasten-Wachstumsfaktor-Rezeptors FGFR1 bei experimenteller autoimmuner Enzephalomyelitis (EAE)

Rajendran, Ranjithkumar


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URN: urn:nbn:de:hebis:26-opus-113581
URL: http://geb.uni-giessen.de/geb/volltexte/2015/11358/

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Freie Schlagwörter (Englisch): EAE , FGF , FGFR1 , oligodendrocytes , MS
Universität Justus-Liebig-Universität Gießen
Institut: Institute of Animal Physiology
Fachgebiet: Biologie
DDC-Sachgruppe: Biowissenschaften, Biologie
Dokumentart: Dissertation
Sprache: Englisch
Tag der mündlichen Prüfung: 19.02.2015
Erstellungsjahr: 2014
Publikationsdatum: 26.02.2015
Kurzfassung auf Englisch: Fibroblast growth factors (FGFs) exert diverse biological effects by binding and activation of specific fibroblast growth factor receptors (FGFRs). Recent studies on the function of FGF2 in MOG35-55-induced experimental autoimmune encephalitis (EAE) showed that systemic deletion of FGF2 leads to a more severe disease course, increased lymphocyte and macrophage infiltration and decreased remyelination. In the present study the in vivo function of the corresponding receptor Fgfr1 was characterized using an oligodendrocyte-specific genetic approach. Plp/CreERT:Fgfr1fl/fl mice were administered tamoxifen to induce conditional Fgfr1 deletion in oligodendrocytes (referred to as Fgfr1ind-/-). In MOG35-55-induced EAE the Fgfr1ind-/- mice show a delayed onset of disease, less maximum disease severity and enhanced recovery. Decreased lymphocyte and macrophage/microglia infiltration, and myelin and axon degeneration are found in Fgfr1ind-/- mice. In acute EAE downregulation of proinflammatory cytokines such as TNF-alpha, IL-1beta and IL-6, in chronic EAE downregulation of the CX3CL1/CX3CR1 pathway is seen in Fgfr1ind-/- mice. Furthermore, increased expression of BDNF, TrkB (neurotrophic tyrosine kinase receptor, type 2) and decreased expression of Lingo-1 are found in Fgfr1ind-/- mice. Fgfr1 ablation in oligodendrocytes showed increased TrkB expression in whole lysate of cortex and spinal cord. These data suggest that impaired signalling via oligodendroglial Fgfr1 has a beneficial effect on MOG35-55-induced EAE. These findings on the oligodendroglial Fgfr1 pathway may offer a new target for developing therapy in multiple sclerosis.
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