Building discontinuous liver sinusoidal vessels

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...

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Bibliographic Details
Published in:The Journal of clinical investigation 2017-03, Vol.127 (3), p.790-792
Main Authors: Griffin, Courtney T, Gao, Siqi
Format: Article
Language:English
Subjects:
Anemia
Animals
Biomedical research
Blood
Bone marrow
Capillaries
Capillaries - embryology
Cell differentiation
Circulatory system
Embryo, Mammalian - embryology
Embryonic development
GATA4 Transcription Factor - genetics
GATA4 Transcription Factor - metabolism
Health aspects
Hematopoietic Stem Cells - metabolism
Humans
Intercellular Junctions - genetics
Intercellular Junctions - metabolism
Liver
Liver - blood supply
Liver - embryology
Mice
Morphology
Neovascularization, Physiologic - physiology
Proteins
Rodents
Spleen
Stem cells
Transcription factors
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Summary: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.
ISSN:0021-9738
1558-8238
DOI:10.1172/JCI92823