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. 2019 Jul 3;33(10):10680–10691. doi: 10.1096/fj.201900070R

Figure 3.

Figure 3

Impaired astrocyte activation and gliosis in GPR37 KO mice after stroke. Immunohistochemical staining measured reactive astrocytes in the ischemic cortex 24 and 72 h after stroke. A) Representative image of GFAP-positive reactive astrocytes in the sham-treated control cortex and the ischemic cortex after stroke. Reactive astrocytes accumulated in the peri-infarct region surrounding the ischemic core (asterisk). These astrocytes showed hypertrophic cell bodies and elongated processes in the WT brain, whereas these morphologic changes associated with astrogliosis were noticeably reduced in GPR37 KO mice. B) Immunostaining images of GFAP-positive astrocytes (red) at 72 h after stroke. There was higher density and greater number of GFAP-positive cells in WT mice next to the ischemic core (asterisk) compared with the GPR37 KO brain. C) Quantification of the GFAP fluorescence at 24 and 72 h after stroke. The increase of fluorescence intensity of reactive astrocytes was significantly less in GPR37 KO mice compared with WT mice (2-way ANOVA; F = 190.4; n = 5). **P < 0.01. D) At 7 d after stroke, we observed dramatically fewer GFAP-positive cells, consistent with the much-weakened glial scar formation at this delayed time point. Mann-Whitney U test nonparametric test was applied for the comparison; n = 5/group. **P = 0.0153 vs. WT stroke controls.