Fig. 6

Glucocorticoids triggers IPAM formation. A Upstream IPA of top 200 differentially expressed genes in IPAM (Fisher’s exact test, Benjamini–Hochberg FDR). B Histograms visualizing targeted metabolomics results in the sham, infarct, and peri-infarct group brain samples from sham and MCAO-12 h mice. n = 6/group. C–D Heatmap showing the expression of several ICAM-specific or IPAM-specific marker genes upon DEX (5 nM, 24 h) (C) or CORT (1 μM, 24 h) (D) stimulation. n = 3/group. E–F TTC staining of brains from CON, CORT, and RU486 group (E). The infarct volume was quantified (F). n = 6/group. G–H mNSS were performed at 1 day (G) and 3 days (H) after MCAO to evaluate the neurological deficits of each group. n = 7–14/group. I Grip strength was performed at 1 day and 3 days after MCAO to evaluate the neurological deficits of each group. n = 7–14/group. J Representative TUNEL images co-stained with neuronal-marker NEUN within the ischemic regions in the MCAO 1d brains from CON, CORT, and RU486 groups (scale bar: 50 µm). K Proportion of TUNEL⁺/NeuN⁺ cells in NeuN⁺ cells was quantified. n = 3/group. L Expression of PIK3IP1 in TMEM119.⁺ cells was quantified. The fluorescence intensity of PIK3IP1 in the CORT and RU486 groups was normalized to the mean value of that measured in the CON group. n = 3/group. M Representative immunostaining of IPAM-specific marker PIK3IP1 and microglia-specific marker TMEM119 in the peri-infarct within MCAO-1d sections from CON, CORT, and RU486 groups (scale bar: 20 µm). In B, F–H, K, and L, one-way ANOVA with Tukey’s post hoc test. In I, two-way ANOVA with Tukey’s post hoc test. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001