Skip to main content
. Author manuscript; available in PMC: 2020 Feb 21.
Published in final edited form as: Cell. 2019 Jan 24;176(5):1128–1142.e18. doi: 10.1016/j.cell.2018.12.023

Figure 6. Endothelial Cxcl12 and Cxcr4 facilitate neonatal heart regeneration. See also Figure S5 and S6.

Figure 6.

(A) Model for collateral formation in neonates upon MI. (B-E) Ejection fractions 28 days post-MI. No decrease in controls (B) (n=8 No-MI, n=14 MI animals). Function is reduced with Pan-EC Cxcl12 deletion (C) (n=12 No-MI, n=9 MI animals) and arterial Cxcr4 deletion (D) (n=8 No-MI, n=8 MI animals) 28 days post-MI. (E) Normal function in non-injured hearts with postnatal endothelial gene deletions. N= 8 controls, n=12 Cxcl12fl/fl; Cdh5CreER, n=8 Cxcr4fl/fl; Cx40CreER animals. (F) Compared to controls (n=12), fibrotic scar was increased in endothelial Cxcl12 (n=11 hearts) and arterial Cxcr4 (n=7 hearts) knockouts. (G) Transverse section indicating ischemic zone, border zone and remote zone. (H) Reduced PH3+ cardiomyocytes in ischemic, border, and remote zone of neonatal hearts lacking endothelial Cxcl12 (n≥5) or arterial Cxcr4 (n=5), 7 days post-MI. lig, ligated; LCA, left coronary artery; RCA, right coronary artery; P, postnatal; Endo, endothelial; EC, endothelial cell; MI, myocardial infarction. Error bars are st dev: *, p≤0.05; **, p≤0.01; ***, p≤0.001, ****, p≤0.0001.