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(Circulation Research. 2003;92:255.)
© 2003 American Heart Association, Inc.

Editorials

The FAKs About Blood Vessel Assembly

Brenda L. Bohnsack, Karen K. Hirschi

From the Departments of Molecular and Cellular Biology (B.L.B., K.K.H.) and Pediatrics (K.K.H.), Center for Cell and Gene Therapy, Children’s Nutrition Research Center, Baylor College of Medicine, Houston, Tex.

Correspondence to Karen K. Hirschi, One Baylor Plaza, N1030, Baylor College of Medicine, Houston, TX 77030. E-mail khirschi@bcm.tmc.edu

Key Words: blood vessels • embryonic development • extracellular matrix • focal adhesion kinase

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The formation of blood vessels during embryonic development is a complex process that requires the coordination of multiple soluble signals, as well as coordinated communication of cells with one another and with their surrounding extracellular matrix (ECM). The process of vessel assembly can be dissected into discernible steps that appear to require unique controls (depicted in the Figure, panel A): induction of mesodermal progenitors to an endothelial fate (differentiation of angioblasts); migration of angioblasts and alignment into a primitive vascular plexus; endothelial tube formation; vascular fusion and plexus remodeling; endothelial cell recruitment of mesenchymal progenitors; and endothelial-induced mural cell differentiation.¹

View larger version (36K): [in this window] [in a new window]   Potential role of FAK in blood vessel assembly. The process of vessel assembly can be dissected into discernible steps (A), and there is evidence to suggest that FAK is involved throughout. In FAK-/- mutants (B), blood vessel assembly is arrested during tubulogenesis, suggesting that the primary role of FAK in vascular development is the control of endothelial cell migration and tube formation or perhaps earlier during mesodermal induction. However, FAK has also been shown to mediate PDGF-B signaling in mural cell proliferation and migration, which is necessary for the formation of stable, quiescent vessel structures. Therefore, FAK may have other later roles in vessel assembly, which are not revealed in the FAK-/- mutants due to early lethality. Col1 indicates type I collagen; Cx, connexin; Fn, fibronectin; IHH, Indian Hedgehog; Lm, laminin; Ptc, Patched; Smo, Smoothened; and Vn, vitronectin.

Studies in genetically malleable model systems have enabled the identification of . . . [Full Text of this Article]

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