Fig. 7: RNA-seq validated that TGF-β pathway is related to BM EPC dysfunction in patients with AA.
From: TGF-β inhibition restores hematopoiesis and immune balance via bone marrow EPCs in aplastic anemia
a, A schematic diagram of the study design for RNA-seq analysis of AA EPCs and NC EPCs. b, A principal component analysis (PCA) of AA EPCs and NC EPCs. c, A heat map of upregulated and downregulated genes in AA EPCs and NC EPCs. d, A KEGG pathway analysis showing that TGF-β pathway was upregulated in AA EPCs. e, A KEGG analysis of enriched pathways in NC EPCs. f,g, The mRNA levels of hematopoietic-related genes in impaired EPC models (f) and in AA EPCs (g). h, A schematic illustration indicating that hyperactive TGF-β signaling pathway with downstream Smad2/3 phosphorylation contributes to dysfunctional BM EPCs in AA, whereas TGF-β inhibition repairs dysfunctional BM EPCs, decreasing apoptosis, increasing angiogenesis and migration, and improving multilineage hematopoiesis and immune balance in vitro and in vivo, providing a potential therapeutic strategy for patients with AA. The data are presented as the mean ± s.e.m. (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001).
