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. 2022 May 25;54:102347. doi: 10.1016/j.redox.2022.102347

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© 2022 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 4 — Prdx1 is essential for SAM activation after stroke damage. (A) UMAP plots showing clusters and annotations of cells identified in Prdx1+/+ and Prdx1−/− IL hemispheres after tMCAO. (39,956 cells) (B) UMAP plots showing immune cells clusters in Prdx1+/+ (WT IL) or Prdx1−/− (KO IL) IL hemispheres at 24 h after tMCAO (left panel). Bar plot showing the relative distribution of each cluster identified in the Prdx1+/+ (WT) and Prdx1−/− IL (KO) hemispheres at 24 h after tMCAO (right panel). (C) Subclustering analysis of the microglia identified in (A). (D) UMAP plots of microglial subclusters in the Prdx1+/+ (WT IL) and Prdx1−/− IL (KO IL) hemispheres (left panel). Stacked bar graph showing the number of microglia counted from the Prdx1+/+ (WT) and Prdx1−/− IL (KO) hemispheres at 24 h after tMCAO (left panel). (E) Projection of microglia on a pseudo-time graph plot displaying the transition from homeostatic microglia (clusters 1 and 2, blue) to SAM (cluster 3, yellow). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)