Additional file 1: of Aryl hydrocarbon receptor modulates stroke-induced astrogliosis and neurogenesis in the adult mouse brain

Figure S1 Representative immunohistochemical staining for AHR intracellular distribution. Depending on the status of AHR expression and the availability of AHR ligands, which is presumably different among cells, AHR ligands would bind to cytoplasmic AHR for its activation and nuclear translocation dynamically. Compared with the normal AHRcKO which had little AHR immunoreactivity (B), the normal AHRflx/flx (A) showed predominantly nuclear distribution of AHR immunoreactivity, and to a lesser extent in the cytoplasm in Iba1-positive and Iba-1 negative cells. Figure S2 The expression levels of 84 candidate genes and 5 housekeeping genes from the ipsilesional hemisphere by neurogenesis array. (A) The array data obtained by real-time polymerase chain reaction (RT-PCR). Changes beyond 1 ± 0.5-fold are shown as differentially expressed genes. The WT-Vehicle group show the upregulated gene expression of S100β, Cxcl1, Bmp2, Tgfβ1, Odz1 and downregulated Mef2c, Ngn2 and Ngn1 at 48 h after MCAO. In contrast, the WT-TMF group downregulated the gene expression of S100β, Cxcl1, Bmp2, Tgfβ1, and Odz1 and upregulated Mef2c, Ngn2 and Ngn1 compared with vehicle treatment after MCAO. (B) On the other hand, in the AhRflx/flx group, upregulated S100β and Cxcl1 gene expression was observed after MCAO. In AhRcKO mice, downregulated S100β and Cxcl1 and upregulated Ngn2, Nr2e3 and Cdk5rap2 gene expression were noted compared with the AhRflx/flx group after MCAO (n = 3/each group). (C) In summary of the 84 gene expression regulation, the common changes by pharmacological inhibition (TMF, marked in blue) and AhRcKO mice (marked in pink) were S100β, Cxcl1, Ngn2, and Ngn1 (marked in purple). #p < 0.05 compared with the respective normals. *p < 0.05 WT-TMF compared with the WT-Vehicle and AhRcKO compared with the AhRflx/flx. (DOCX 1757 kb)