Fig 2: LEC Sorting from Human LNs for Single-Cell AnalysisGating strategy for isolation of LECs from human LNs. CD45+ cells and dead cells are excluded based on CD45 and Live/Dead dead cell stain, respectively. Live single CD45-PDPN+CD31+ are sorted for the single-cell analysis of human LECs. Adopt from Figure S1A of Takeda et al., 2019.

Fig 3: Baseline aCECs levels of placebo group and anlotinib group. A, CD31‐labeled aCECs levels of the two groups. B, CD105‐labeled aCECs levels of the two groups. aCECs, activated circulating endothelial cells

Fig 4: Defined surfaceome transcript of the developing epicardium revealed the enrichment of CD22 and CDH18 in late-stage populations.a PCA using the GSE84085 RNA-Seq expression dataset of d12 early epicardial-like cells (Epi12, red) (19-9-7-Epi, n = 2), d48 late epicardial-like cells (Epi48, brown) (H9-Epi, ES03-Epi and 19-9-11-Epi, n = 6) and human adult epicardium (dark violet) (donors 9605, 9633, 9634 and 9635, n = 8). b Venn-Diagram showing genes in significant absolute correlation to the epicardial markers WT1 (light green), TBX18 (light pink) and ALDH1A2 (light purple) (Pearson correlations; R ≥ 0.6) as well as cell surface marker enrichment (target). c Overlap of the target gene set from b (gray) against DEGs (Supplementary Fig. 1e) (light brown) for the surfaceome transcript identification of the epicardium. d Heatmap showing correlations (Pearson, R, 1 to −0.7, color scale) of surface marker expression relative to the expression of endothelial cell markers CDH5 and PECAM1. e Fold change of surface marker expression in Epi48 (brown) relative to Epi12 (red). f Heatmap showing correlations (Pearson, R, 0.6–1, color scale) of the top three genes from (e) to epicardial markers. g Retrospective analysis showing a heatmap depicting active epicardial markers and CD22 and CDH18 expression in embryonic and adult cells. h Analysis for CD22 and CDH18 expression in CF (left) and SMC (right) with representative CF genes (yellow) and SMC genes (light blue) [error bars indicate standard derivation (SD)]. i Heatmap showing correlations (Pearson, R, 0 to −1, color scale) of CD22 and CDH18 for CF markers PDGFRA, FAP and POSTN and SMC markers CNN1, ACTA2, and TAGLN. j GSE106168 retrospective analysis for CDH18 expression in different cardiac cellular clusters [(C1—5W whole heart (n = 257); C2—Cardiomyocytes (n = 1492); C3—fibroblast-like cells (n = 786); C4—endothelial cells (n = 445); C5—heart valves (n = 427); C6—epicardial -EPI- cells (n = 46); C7—immune cells (n = 27); C8—macrophages (n = 308); C9—T and B lymphocytes (n = 58)] k GSE106168 retrospective analysis for CDH18 expression in epicardial-EPI-cluster [UPK3Bhigh WT1high TBX18high ALDH1A2high] ranging different time points of gestation [5 weeks, n = 30; 22 weeks, n = 46].

Fig 5: Identification and differentiation potential of CAFs isolated from HCC tissues.A HCC tissues and matching tumor-adjacent tissues were subjected to H&E staining respectively (upper); IHC images showed α-SMA expression respectively (lower). The red arrows indicated α-SMA positive cells. Scale bar: 100 μm. B The images showed representative morphology of CAFs and PTFs in vitro. The isolated CAFs and PTFs were treated with adipogenic induction and stained by Oil Red O. And CAFs and PTFs were treated with osteogenic induction and stained by Alizarin Red S. Scale bar: 100 μm. C Immunofluorescence staining of CAFs and PTFs showed α-SMA, Vimentin positive expression and E-cadherin, CD31 negative expression. Scale bar: 100 μm. D Flow cytometric analysis showed CAFs were positive for CD105, CD73, CD90, and CD44, negative for CD31, CD34, CD45, and HLA-DR.