Figure 2
Figure 2. Compounds affecting distinct aspects of blood vessel development in vivo. Compound-treated (A-N) and control (DMSO-treated) Xenopus embryos (O-P) were analyzed by whole-mount in situ hybridization for expression of the vascular marker gene apj. Stage 35/36 embryos are shown in lateral views with anterior to the left. Close-up views of the trunk illustrate the morphology of the blood vessels. Compound names are indicated. (A-D) Hypoplastic VVN (*) and PCV (arrowheads). (E-F) Lack of ISVs (arrowheads). Note that assembly of PCVs and VVN (*) is unaffected. (G-H) Ectopic ISVs (arrowheads) and dysplastic VVN (*). (I-J) Ectopic ISV (arrowheads) and hyperplastic VVN (*). (K-N) Hypoplastic, dispersed VVN (*), but normal ISV angiogenesis (arrowheads). (O-P) Control embryos with normal VVN (*), PCVs (arrow), and ISVs (arrowhead). (Q) Scheme of the blood vasculature (blue) of the stage 35/36 embryo. Calmidazolium indicates calmidazolium chloride; Indirubin, indirubin-3′-oxime; and PS, pronephric sinus.

Compounds affecting distinct aspects of blood vessel development in vivo. Compound-treated (A-N) and control (DMSO-treated) Xenopus embryos (O-P) were analyzed by whole-mount in situ hybridization for expression of the vascular marker gene apj. Stage 35/36 embryos are shown in lateral views with anterior to the left. Close-up views of the trunk illustrate the morphology of the blood vessels. Compound names are indicated. (A-D) Hypoplastic VVN (*) and PCV (arrowheads). (E-F) Lack of ISVs (arrowheads). Note that assembly of PCVs and VVN (*) is unaffected. (G-H) Ectopic ISVs (arrowheads) and dysplastic VVN (*). (I-J) Ectopic ISV (arrowheads) and hyperplastic VVN (*). (K-N) Hypoplastic, dispersed VVN (*), but normal ISV angiogenesis (arrowheads). (O-P) Control embryos with normal VVN (*), PCVs (arrow), and ISVs (arrowhead). (Q) Scheme of the blood vasculature (blue) of the stage 35/36 embryo. Calmidazolium indicates calmidazolium chloride; Indirubin, indirubin-3′-oxime; and PS, pronephric sinus.

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