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Effects of fingolimod on astrocyte activation and glutamate transporter mRNA levels in the spinal cord during EAE.

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posted on 08.03.2017, 18:30 by De-Hyung Lee, Silvia Seubert, Konstantin Huhn, Lukas Brecht, Caroline Rötger, Anne Waschbisch, Johannes Schlachetzki, Alice Klausmeyer, Arthur Melms, Stefan Wiese, Jürgen Winkler, Ralf A. Linker

(A, B) Representative GFAP staining of spinal cord cross sections from a mouse treated with fingolimod in a preventive setting and a sham treated control at the maximum of EAE. Note the reduced GFAP staining after fingolimod treatment. Bar = 100µm (C) Blinded quantification of GFAP immunreactivity as marker of astrocyte activation on spinal cord cross sections. (D) RT-PCR analysis of slc1a2 expression. (E) RT-PCR analysis of slc1a3 expression, n = 6–8 per group. The mRNA expression of a prophylactically treated mouse is set to 1 as reference. All data are given as mean ± SEM. Please note that data are compiled from separate experiments with different starting points of fingolimod application (d0, 11 or 25). The day (d) on the X axis indicates the start of treatment directly after immunization (d0, n = 6 mice per group), at the first sign of symptoms (d11, n = 6 mice per group) or at the early chronic phase of the disease (d25, n = 8 mice per group). Experiments were analysed at the maximum of disease (days 15 or 17 p.i., respectively) for treatment start on day 0 and 11 p.i. and in the later chronic phase of EAE (day 80 p.i.) after treatment start on day 25 p.i. * p < 0.05, ** p < 0.01; *** p < 0.001, Mann Whitney test.

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