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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: Stroke. 2021 May 4;52(7):2381–2392. doi: 10.1161/STROKEAHA.120.033547

Fig. 6: FosDT deletion regulated post-stroke pathological changes.

Fig. 6:

Gene Set Enrichment Analysis (GSEA) of DETs between FosDT−/− MCAO vs. FosDT+/+ MCAO groups showed various up- and downregulated pathways (A). Gene ontology (GO) analysis and KEGG pathways analysis also showed the response of various pathways, including inflammation in FosDT−/− rats compared to FosDT+/+ rats after focal ischemia (B). Immunostaining decreased apoptosis (cleaved casp-3), mitochondrial dysfunction (pDrp1), and oxidative stress (3-NT) in the NeuN+ cells (neuronal) in the cortical peri-infarct region of FosDT−/− and FosDT+/+ rats at 24h of reperfusion after 60 min of transient MCAO (n=3/group) (C). Blue is DAPI for nuclei. PTM, post-translation modification; Cleaved casp-3, Cleaved caspase-3; pDrp1, phosphorylated dynamin-related protein-1 and 3-NT, 3-nitrotyrosine. Scale bar=50 μm.