Targeted deletion of BMK1/ERK5 in adult mice perturbs vascular integrity and leads to endothelial failure
J. Clin. Invest. Masaaki Hayashi, et al. 113:1138 doi:10.1172/JCI19890 [
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Figure 6Essential role of BMK1 in ECs but not in cardiomyocytes during embryogenesis. (A–C) Growth retardation of global BMK1-KO (
BMK1–/–) and endothelial-specific BMK1-KO (BMK1-ecKO) embryos. Gross appearance of yolk sacs (left panel) and embryos (right panel) from WT (A),
BMK1–/– (
–/–) (B), and BMK1-ecKO (ecKO) (C) mutants at E9.5 are shown. Arrow in A indicates the major vitelline vessels, which are barely detectable in
BMK1–/– and BMK1-ecKO mutants. (D–F) H&E staining of yolk sac of WT (D),
BMK1–/– (E), and BMK1-ecKO (F) mutants at E9.5. Note that the vessels of the
BMK1–/– and BMK1-ecKO yolk sacs are dilated compared with the vessels of the WT yolk sac. Asterisk denotes the underdeveloped vessels. (G–I) H&E staining of that hearts of WT (G),
BMK1–/– (H), and BMK1-ecKO (I) mutants at E9.5. Arrowheads indicate ECs. (J) Deficit in endothelial proliferation in BMK1-ecKO heart explant cultures. (K and L) H&E staining of sections from WT and BMK1-cmKO (cmKO) hearts. M, myocardium; VE, visceral endoderm. Scale bars: D–I, K, and L, 10 μm.
