40478_2018_606_MOESM3_ESM.tif (14.86 MB)
Additional file 3: of Modulation of astrocyte reactivity improves functional deficits in mouse models of Alzheimer’s disease
figure
posted on 2018-10-16, 05:00 authored by Kelly Ceyzériat, Lucile Ben Haim, Audrey Denizot, Dylan Pommier, Marco Matos, Océane Guillemaud, Marie-Ange Palomares, Laurene Abjean, Fanny Petit, Pauline Gipchtein, Marie-Claude Gaillard, Martine Guillermier, Sueva Bernier, Mylène Gaudin, Gwenaëlle Aurégan, Charlène Joséphine, Nathalie Déchamps, Julien Veran, Valentin Langlais, Karine Cambon, Alexis Bemelmans, Jan Baijer, Gilles Bonvento, Marc Dhenain, Jean-François Deleuze, Stéphane Oliet, Emmanuel Brouillet, Philippe Hantraye, Maria-Angeles Carrillo-de Sauvage, Robert Olaso, Aude Panatier, Carole EscartinFigureS2. Unlike STAT3, STAT1 and Erk are not activated in APP astrocytes. Confocal images of stained hippocampal sections from 12-month-old WT-GFP, APP-GFP and APP-SOCS3 mice. a, GFP+ astrocytes (green) stained for GFAP (magenta) and STAT3 (cyan). APP astrocytes are reactive (hypertrophic and GFAP overexpression). They display STAT3 nuclear accumulation. SOCS3 reduces GFAP and STAT3 expression in APP mice, even around amyloid plaques (star). b, Quantification of STAT3 immunoreactivity in astrocyte soma. N = 5–7/group. One way ANOVA and Tukey’s post hoc test. *** p < 0.001. c-d, Sections stained in magenta for STAT1 (c) or P-ERK (d), DAPI (blue) and GFP (green). STAT1 and P-ERK are not induced in APP reactive astrocytes while CNTF induces significant STAT1 nuclear accumulation (c) and LPS triggers ERK phosphorylation (d). DAPI stains nuclei as well as amyloid plaques. Representative images from N = 4–6/group. (TIF 15218 kb)
