Vascular Development and Differentiation During Human Liver Organogenesis

Collardeau-Frachon, Sophie; Scoazec, Jean‐Yves

doi:10.1002/ar.20679

Cited by 154 publications

(130 citation statements)

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“…In the present study, three HVs were observed in 68.4% of the cases after CS15, indicating that the three HVs are acquired around CS15 in most cases. These data are consistent with those of a previous study reporting profound remodeling of the efferent venous system during the 5th gestational week (Dickson, 1957;Collardeau-Frachon and Scoazec, 2008). Three HVs were not identified until after CS17 in 19.6% of cases, suggesting that there are several individual variations in the number and arrangement of the terminal HVs, in contrast to the afferent venous circulation systems.…”

Section: The Morphology and Morphometry Of Embryonic Liversupporting

confidence: 92%

“…Original and first-hand data regarding the stages of development of the vascular architecture of the liver are scarce (Collardeau-Frachon and Scoazec, 2008). Though the asymmetry of the hepatic vascular structure may be acquired between CS13 and CS16, the precise stages of development could not be determined.…”

Section: The Morphology and Morphometry Of Embryonic Livermentioning

confidence: 99%

“…The liver lies at an active center of angiogenesis in the early embryonic period. The asymmetricity of the afferent venous vessels of the liver derives from two specific circulation systems: the vitelline and umbilical veins, which are acquired between CS13 and CS16 (Mall, 1906;Dickson, 1957;Collardeau-Frachon and Scoazec, 2008). Efferent venous vessels, including the right, left, and middle hepatic veins (HVs) and the inferior vena cava (IVC), form at similar stages.…”

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confidence: 99%

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Embryonic Liver Morphology and Morphometry by Magnetic Resonance Microscopic Imaging

Hirose

Nakashima

Yamada

et al. 2011

The Anatomical Record

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Embryonic liver has a unique external morphology and quantitative morphometry, based on magnetic resonance imaging data of human embryos from the Kyoto Collection of Human Embryos. Liver morphogenesis is strongly affected by the adjacent organs and tissues. The left ventricle develops to the left medial-caudal side, which results in the formation of a depression at left medial region and a prominence bilaterally at the cranial surface of the liver between Carnegie Stage (CS)17 and CS19. An imprint of the stomach that formed at the dorsal left-medial region of the liver became more marked with development until CS23. A depression induced by the umbilicus formed at the ventral region of the liver between CS16 and CS19. An indentation caused by the right adrenal gland formed at the dorsal-caudal region of the liver surface from CS20. Morphometric analysis revealed that the volume of the liver increased exponentially from CS14 through CS23. The liver developed preferentially along the dorsoventral axis and right/left axis until CS17, along the craniocaudal axis between CS17 and CS19, and then in all directions after CS19. Several important developmental phenomena, such as differentiation of the diaphragm, the extension of the body axis of the embryo, and the physiologic herniation of the intestine into the umbilical cord, may affect morphometric data. These data contribute to a better understanding of liver development as well as the morphogenesis of adjacent organs, both temporally and spatially, and serve as a useful reference for fetal medicine and prenatal diagnosis. Anat Rec, 295:51-59, 2012. V V C 2011 Wiley Periodicals, Inc.

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Section: The Morphology and Morphometry Of Embryonic Liversupporting

confidence: 92%

Section: The Morphology and Morphometry Of Embryonic Livermentioning

confidence: 99%

mentioning

confidence: 99%

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Embryonic Liver Morphology and Morphometry by Magnetic Resonance Microscopic Imaging

Hirose

Nakashima

Yamada

et al. 2011

The Anatomical Record

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“…The observed abnormalities are in line with the expression pattern of Plexin-B2 in the highly specialized discontinuous endothelium of the liver. During both development and liver regeneration in the adult, the hepatic portal veins and sinusoids derive from preexisting vessels through angiogenesis (54,55). There is evidence that RhoA activation downstream of Plexin-B1 stimulates cellular processes in endothelial cells that are crucial for angiogenesis, including chemotactic migration and tubulogenesis (56).…”

Section: Discussionmentioning

confidence: 99%

Genetic dissection of plexin signaling in vivo

Worzfeld

Swiercz

Sentürk

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Mammalian plexins constitute a family of transmembrane receptors for semaphorins and represent critical regulators of various processes during development of the nervous, cardiovascular, skeletal, and renal system. In vitro studies have shown that plexins exert their effects via an intracellular R-Ras/M-Ras GTPase-activating protein (GAP) domain or by activation of RhoA through interaction with Rho guanine nucleotide exchange factor proteins. However, which of these signaling pathways are relevant for plexin functions in vivo is largely unknown. Using an allelic series of transgenic mice, we show that the GAP domain of plexins constitutes their key signaling module during development. Mice in which endogenous Plexin-B2 or Plexin-D1 is replaced by transgenic versions harboring mutations in the GAP domain recapitulate the phenotypes of the respective null mutants in the developing nervous, vascular, and skeletal system. We further provide genetic evidence that, unexpectedly, the GAP domain-mediated developmental functions of plexins are not brought about via R-Ras and M-Ras inactivation. In contrast to the GAP domain mutants, Plexin-B2 transgenic mice defective in Rho guanine nucleotide exchange factor binding are viable and fertile but exhibit abnormal development of the liver vasculature. Our genetic analyses uncover the in vivo contextdependence and functional specificity of individual plexin-mediated signaling pathways during development.neural tube | cerebellum | outflow tract P lexins constitute a family of transmembrane proteins that serve as receptors for semaphorins (1). They function as key regulators of a multitude of developmental processes, including axon guidance, pattern and synapse formation in the nervous system (2), vasculogenesis and angiogenesis (3, 4), and morphogenesis of the heart, kidney, and skeletal system (5). In the adult organism, plexins play crucial roles in the physiology and pathophysiology of the immune and cardiovascular system, as well as in bone homeostasis and in cancer (6-9). Nine plexins have been identified in the mammalian system, which are grouped into four subfamilies, A-D, according to sequence homologies.The activation of plexins by their semaphorin ligands triggers several intracellular signaling cascades, most of which modulate the activity of small GTPases (10). The intracellular domain of all plexins shares homology with GTPase-activating proteins (GAPs) and confers the deactivation of R-Ras, M-Ras, and Rap1 (11-17). The GAP activity toward R-Ras and M-Ras, but not toward Rap1, requires binding of Rnd GTPases to the plexin receptor (11,12,15,16). Plexins of the B-subfamily differ from all other plexins in that they carry a C-terminal PDZ domain interaction motif that mediates a stable interaction with the Rho guanine nucleotide exchange factor (RhoGEF) proteins . Activation of B-plexins by semaphorin ligands results in activation of the RhoGEF proteins and subsequent activation of . This process and the GAP function of B-plexins are independent of each other, becau...

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“…This venous system transports the splanchnic venous flow through the portal vein to the liver [1,6]. The afferent venous circulation of the liver as well as its efferent venous system, i.e., the hepatic veins, derives from an extraembryonic venous system, the vitelline venous system, which transports blood from the yolk sac to the heart at the end of the 3rd week of gestation [7]. This extraembryonic origin of the portal system perhaps determines some of the pathological evolutive characteristics when it suffers hyperpressure.…”

Section: Introductionmentioning

confidence: 99%

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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Vascular Development and Differentiation During Human Liver Organogenesis

Cited by 154 publications

References 50 publications

Embryonic Liver Morphology and Morphometry by Magnetic Resonance Microscopic Imaging

Embryonic Liver Morphology and Morphometry by Magnetic Resonance Microscopic Imaging

Genetic dissection of plexin signaling in vivo

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

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