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. 2023 May 8;24(7):e56030. doi: 10.15252/embr.202256030

Figure EV5. ScRNA‐seq analysis on the small intestines from control and EC‐Foxc‐DKO mice 18.5 h after I/R.

Figure EV5

  1. Pie chart showing the percentage of each cell cluster identified in Fig 6A of total cell population.
  2. Sub‐clustering performed on the cluster 20 (Telocytes/Trophocytes).
  3. Dot plot showing relative expression of different genes identified by scRNA‐seq were decreased in crypt cell cluster in EC‐Foxc‐DKO mice compared with control mice at I/R‐18.5 h. Fill colors represent normalized mean expression levels and circle sizes represent the within‐cluster frequency of positive gene detection. Lgr5, Olfm4, Ascl2, Sox9, Cd24a, Smoc2 and Aldh1b1 are ISC markers. Mik67 is a proliferative marker. Ascl2, Sox9 and Axin2 are Wnt/β‐catenin target genes.
  4. Schematic drawing of the mechanism by which endothelial FOXC1 and FOXC2 promote mouse intestinal regeneration after I/R injury. The intestinal mucosa is damaged after I/R injury. FOXC (both FOXC1 and FOXC2) regulate the expression of Rspo3/Cxcl12 through binding to their regulatory elements in LECs/BECs of the lymphatic/blood vessels near the crypts, respectively. RSPO3 secreted by LECs (blue arrow) is an agonist of the canonical Wnt/β‐catenin signaling pathway and promotes the intestinal epithelial regeneration and repair. RSPO3 derived from LECs also promotes angiogenesis and lymphangiogenesis (dashed arrows). BEC‐derived CXCL12 (pink arrow) not only regulates angiogenesis (arrow) but also stimulates CXCR4 on LECs to enhance lymphangiogenesis (dashed arrow). L, lymphatic vessel; B, blood vessel; ISC, intestinal stem cell; LEC, lymphatic endothelial cell; BEC, blood endothelial cell.

Source data are available online for this figure.