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Building discontinuous liver sinusoidal vessels
Courtney T. Griffin, Siqi Gao
Courtney T. Griffin, Siqi Gao
Published March 1, 2017; First published February 20, 2017
Citation Information: J Clin Invest. 2017;127(3):790-792. https://doi.org/10.1172/JCI92823.
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Category: Commentary

Building discontinuous liver sinusoidal vessels

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Abstract

Blood vessels have a unified mission to circulate blood throughout the body; however, they have additional diverse and specialized roles in various organs. For example, in the liver, discontinuous sinusoids, which are fenestrated capillaries with intercellular gaps and a fragmented basement membrane, facilitate delivery of macromolecules to highly metabolic hepatocytes. During embryonic development, discontinuous sinusoids also allow circulating hematopoietic progenitor and stem cells to populate the liver and promote blood cell differentiation. In this issue of the JCI, Géraud et al. describe an essential role for the transcription factor GATA4 in promoting the development of discontinuous sinusoids. In the absence of liver sinusoidal GATA4, mouse embryos developed hepatic capillaries with upregulated endothelial cell junction proteins and a continuous basement membrane. These features prevented hematopoietic progenitor cells from transmigrating into the developing liver, and Gata4-mutant embryos died from subsequent liver hypoplasia and anemia. This study highlights the surprising and extensive transcriptional control GATA4 exercises over specialized liver vascular development and function.

Authors

Courtney T. Griffin, Siqi Gao

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Figure 1

Gata4 deletion alters liver sinusoid morphology.

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Gata4 deletion alters liver sinusoid morphology.
Genetic deletion of th...
Genetic deletion of the transcription factor Gata4 from liver sinusoidal endothelial cells (LSECs) causes upregulation of endothelial cell junction proteins and robust deposition of basement membrane proteins that prevent circulating hematopoietic progenitor or stem cells from colonizing the fetal liver (11). The consequences of this transition from discontinuous sinusoidal to continuous capillary morphology are liver hypoplasia, anemia, and lethality of Gata4 mutant embryos (11).
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