FIGURE

Fig. 7

ID

ZDB-FIG-100128-23

Publication

Mitchell et al., 2010 - Effect of Vascular Cadherin Knockdown on Zebrafish Vasculature during Development

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Fig. 7

Loss of VE-cadherin produces defective endocardial junctions and increased permeability:

Images obtained by transmission electron microscopy of control (a–f) and VE-cad knockdown (g–l) embryos at 48 hpf. The atria of control embryos (a) demonstrate a modest layer of cardic jelly (CJ) between the endocardial (EC) and myocardial layers (MC) (arrowheads are endothelial cell nuclei in a). Knockdown embryos (g) show a stretched myocardium, wide endocardial/myocardial separation and decreased electron density of the cardiac jelly. Mature-appearing, long endocardial junctions are present in controls (between arrowheads, b and c; arrows e). VE-cad MO embryos have smaller, fewer, less well-developed junctions (solid arrows i–k) and endothelial gaps (dashed arrow, i). Both control and knockdown embryos (f and l) demonstrate similar overall numbers of well-developed contractile elements in their myocardial layers (f and l).

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	AB + MO5-cdh5
Knockdown Reagent:	MO5-cdh5
Observed In:	atrial endocardium atrial endocardium cell-cell junction atrial myocardium cardiac jelly
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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