doi: 10.1161/01.RES.0000217601.30361.b1
© 2006 American Heart Association, Inc.
Editorials |
Fishing for Function in Zebrafish
From the Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine, Rochester, NY.
Correspondence to Joseph M. Miano, University of Rochester School of Medicine, 601 Elmwood Ave, Rochester, New York 14642. E-mail j.m.miano@rochester.edu
See related article, pages 846–855
Key Words: smooth muscle • zebrafish • morpholino • acetyltransferase • rapamycin
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Zebrafish have emerged as a powerful and inexpensive vertebrate model system to study the regulation and function of genes. Though this model has been under investigation for more than half a century,1 97% of the published work relating to zebrafish has accumulated in only the last 15 years (Figure). Two important developments have facilitated the rapid ascent of zebrafish as a model system, particular for vascular biology. First, forward genetic screens in zebrafish identified a number of fascinating vascular phenotypes such as gridlock (aortic coarctation) and cloche (loss of endothelial cells [ECs]).2,3 Second, microangiography, coupled to transgenic lines of fish carrying an endothelial cell promoter–driven reporter (eg, green fluorescent protein, GFP), has allowed for the mapping of the zebrafish vasculature in stunning detail with never-before-seen vascular processes amenable to real time visualization.4 These technologies, and evolving tools in reverse genetics, have led to the identification of numerous genes linked to vascular pathology, some of which phenocopy diseases seen in humans (Table). As the Table indicates, essentially all of the zebrafish vascular phenotypes involve perturbations in endothelial cell differentiation, migration, and vascular tube formation with little insight into the role of supportive smooth muscle cells (SMCs). Difficulty in assessing vascular SMC biology in zebrafish stems from our incomplete understanding of the timing of SMC recruitment to the vessel wall, the extent of SMC investment, and the notable lack of SMC markers. Thus, to realize the full potential of zebrafish as a model for vascular biology, developments in
Related Article:
Circ. Res. 2006 98: 846-855.