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. 2022 Sep 15;140(11):1263–1277. doi: 10.1182/blood.2022015499

Figure 1.

Figure 1.

Altered gene expression profiles in HSCs derived from physioxia and ambient air exposure as assessed by CITE-seq analysis. Three biological replicates are analyzed. (A) CITE-seq and cell hashing workflow under physioxia and ambient air. (B) UMAP of CITE-seq data colored by computationally predicted cell clusters. LSK cell types can be discerned by their surface protein marker expression profiles: (1) CD150-CD117-air, (2) CD150-CD117-physioxia, (3) CD150-CD117-physioxia, (4) CD150-CD117-CD48-physioxia, (5) CD150-CD117-CD48-air, (6) CD150 high-physioxia, (7) CD150 high-air, (8) CD150 very high-physioxia, (9) CD150 very high-air, (10) CD48 high-physioxia, (11) CD48 high-air, (12) CD48 mid-air. (C) UMAP of WT BM CD150hi cells under physioxia and ambient air. (D) Heatmap of averaged expression level of HSC renewal and marker genes in WT CD150hi cells under physioxia and ambient air. (E) GSEA plots of selected differentially expressed pathways in WT CD150hi cells under physioxia and ambient air. (F) Heatmap of averaged expression level and GSEA of genes in the p38 MAPK pathway in WT CD150hi cells under physioxia and ambient air. (G) The violin plots show the normalized expression of Tet2 in WT LSK CD150hi cells under physioxia and ambient air. (H) 5-hmC levels in WT BM Lin− cells under physioxia and ambient air; data are presented as mean ± standard error of the mean. ****P < .0001 when analyze by Wilcoxon rank sum test (G) and Student t test (H). KEGG, Kyoto Encyclopedia of Genes and Genomes; PID, The Pathway Interaction Database; UMAP, Uniform Manifold Approximation and Projection.