Academic literature on the topic 'Caudal vein plexus'

Intussusceptive pillars, regarded as a hallmark of intussusceptive angiogenesis, have been described in developing vasculature of many organs and organisms. The aim of this study was to resolve the question about pillar formation and their further maturation employing zebrafish caudal vein plexus (CVP). The CVP development was monitored by in vivo confocal microscopy in high spatio-temporal resolution using the transgenic zebrafish model Fli1a:eGPF//Gata1:dsRed. We tracked back the formation of pillars (diameter ≤ 4 µm) and intercapillary meshes (diameter > 4 µm) and analysed their morphology and behaviour. Transluminal pillars in the CVP arose via a combination of sprouting, lumen expansion, and/or the creation of intraluminal folds, and those mechanisms were not associated directly with blood flow. The follow-up of pillars indicated that one-third of them disappeared between 28 and 48 h post fertilisation (hpf), and of the remaining ones, only 1/17 changed their cross-section area by >50%. The majority of the bigger meshes (39/62) increased their cross-section area by >50%. Plexus simplification and the establishment of hierarchy were dominated by the dynamics of intercapillary meshes, which formed mainly via sprouting angiogenesis. These meshes were observed to grow, reshape, and merge with each other. Our observations suggested an alternative view on intussusceptive angiogenesis in the CVP.

Abstract Introduction and Materials and Methods: Sengis are testicondid, monogamous afrotherian mammals. The testes, pattern of testicular blood vessels and anatomical disposition of caudal vena cava were examined macroscopically in the rufous sengi (Elephantulus rufescens). Testicular structure was further studied microscopically and its components quantified using stereology. Results: The testes were cylindrical in shape and located caudolateral to the kidneys. The testicular arteries branched from renal arteries, ran to the respective testicles without close association with other vessels, while the veins ran straight to the caudal vena cava without pampiniform plexus or intimate association with cognate arteries. There were two caudal vena cavae that united after receiving the renal veins. The seminiferous tubules were bound by a peritubular boundary tissue with a single layer of myoid cells while the interstitial tissue had polyhedral or elongate Leydig cells and connective tissue elements. The testicular volume was estimated at 0.089 ± 0.0031 cm3 with the seminiferous tubules (mean diameter = 210 ± 5.7 μm) constituting 89.4 ± 0.8% of its volume and tubulosomatic index of 0.38%. The interstitial tissue and tunica albuginea constituted 8.9 ± 0.81% and 1.7 ± 0.1% of the testis volume respectively. Conclusion: The testis exhibited general mammalian features while its vascular pattern was simple without indications of a role in testicular thermoregulation as is the case for other afrotherians. The investment of body mass in seminiferous tubules suggests a spermatogenic activity higher than expected in monogamous animals. The double caudal vena cava could be a result of retention of the left supracardinal vein to adulthood.

Angiogenesis is a precise process mediated by a variety of signals and the environmental niche. Although the essential trace element zinc and its homeostasis are essential for maintaining proper cellular functions, whether zinc plays a role in angiogenesis is currently unknown. Using zebrafish embryos as a model system, we found that zinc treatment significantly increased the expression of the slc39a5 gene, which encodes the zinc transporter Slc39a5. Moreover, knocking down slc39a5 expression using either a morpholino or CRISPR/Cas9-mediated gene editing led to cardiac ischaemia and an accumulation of red blood cells in the caudal vein plexus (CVP), as well as delayed venous sprouting and fewer vascular loops in the CVP region during early development. Further analysis revealed significantly reduced proliferation and delayed cell migration in the caudal vein of slc39a5 morphants. At the mechanistic level, we found increased levels of systemic zinc in slc39a5 -deficient embryos, and chelating zinc restored CVP development. In addition, we found that zinc overload in wild-type embryos leads to impaired CVP formation. Taken together, these results indicate that Slc39a5 plays a critical role in endothelial sprouting and migration in venous angiogenesis by regulating zinc homeostasis.

Abstract BACKGROUND The inferior petroclival vein (IPV) courses along the extracranial surface of the petroclival fissure. It is occasionally involved in vascular diseases and has recently been used for vascular access to the cavernous sinus. However, detailed descriptions of its anatomy are currently lacking. OBJECTIVE To define the anatomic relationship between the IPV and its surrounding structures based on cadaveric dissection and radiological analysis. METHODS A dry skull and an injected cadaver head were examined to reveal the relationships between the IPV and its surrounding structures. The existence of the IPV and its relationships with other venous structures were also examined by contrast-enhanced, fat-suppressed T1-weighted magnetic resonance imaging in 26 patients (51 sides). RESULTS The entire course of the IPV was shown via stepwise cadaver dissection from below. Its relationships with surrounding structures, such as the jugular bulb, sigmoid sinus, inferior petrosal sinus, petrosal venous confluence, and the posterior, lateral, and anterior condylar veins, were also shown. In the radiological analysis, the IPV was identified on all sides. The rostral end of the vein was connected to the venous plexus around the carotid artery on all sides. The vein drained into the caudal end of the inferior petrosal sinus (49/51 sides, 96.1%) or into the anterior condylar vein (2/51 sides, 3.9%). CONCLUSION A precise understanding of the anatomy of the IPV will enable endovascular and skull base surgeons to achieve diagnoses and gain safe access to lesions involving the IPV.

Recent studies have focused on capillary pruning in various organs and species. However, the way in which large-diameter vessels are pruned remains unclear. Here we show that pruning of the zebrafish caudal vein (CV) from ventral capillaries of the CV plexus in different transgenic embryos is driven by endothelial cell (EC) rearrangement, which involves EC nucleus migration, junction remodeling, and actin cytoskeleton remodeling. Further observation reveals a growing difference in blood flow velocity between the two vessels in CV pruning in zebrafish embryos. With this model, we identify the critical role of Kruppel-like factor 6a (klf6a) in CV pruning. Disruption of klf6a functioning impairs CV pruning in zebrafish. klf6a is required for EC nucleus migration, junction remodeling, and actin cytoskeleton dynamics in zebrafish embryos. Moreover, actin-related protein transgelin 2 (tagln2) is a direct downstream target of klf6a in CV pruning in zebrafish embryos. Together these results demonstrate that the klf6a-tagln2 axis regulates CV pruning by promoting EC rearrangement.

Genetic regulation of vascular patterning is not fully understood. Here, we report a novel gene, gtpbp1l (GTP-binding protein 1-like), that regulates vascular development in zebrafish. Amino acid sequence comparison and a phylogenetic study showed that gtpbp1l is conserved in vertebrates. Gtpbp1l mRNA is expressed in the vasculature during embryogenesis. Knockdown of gtpbp1l by morpholino impairs the patterning of the intersegmental vessel (ISV) and caudal vein plexus (CVP), indicating the role of gtpbp1l in vasculature. Further apoptosis assays and transgenic fish tests suggested that vascular defects in gtpbp1l morphants are not due to cell death but are likely caused by the impairment of migration and proliferation. Moreover, the altered expression of vessel markers is consistent with the vascular defects in gtpbp1l morphants. Finally, we revealed that gtpbp1l is regulated by VEGF/notch and BMP signaling. Collectively, these findings showed that gtpbp1l plays a critical role in vascular patterning during zebrafish development.

Abstract Background: ADAMTS (a disintegrin and metalloproteinase with thrombospondin motif) members play crucial role in development, inflammation, cancer, and vascular biology. ADAMTS18 is an orphan ADAMTS for which substrates have yet to be discovered. Using ADAMTS18 knock-out (KO) mice, we demonstrated that ADAMTS18 deficiency in mice generated abnormal vascular phenotypes in particular in common carotid artery that is associated with aggravated thrombosis and ischemic cerebral stroke (Blood 122: 31, 2013). Methods and Results: Here, we further investigated the role of ADAMTS18 in angiogenesis. In an established in vivo angiogenesis model (Matrigel plug assay), ADAMTS18 KO mice showed significantly reduced neovessel formation compared to WT mice (Hemoglobin: WT vs. KO, 76.25 ± 28.8 vs. 50.5 ± 17.4, P = 0.048). To systematically evaluate the effect of ADAMTS18 on embryo angiogenesis, we developed zebrafish ADAMTS18 morpholino (MO) knock-down model. Images of trunk regions were taken at 48-hpf (hours post fertilization) with the vascular structures visualized by eGFP fluorescence. Labeled ISV (intersegmental vessel) and DLAV (dorsal longitudinal anastomotic vessel) showed regular development in the embryo injected with control MO. However, embryos injected with ADAMTS18-e3i3-MO presented a lower number of incomplete and thinner ISVs and ectopic sprouts of dorsal aorta. Additionally, ADAMTS18 knock down impaired formation of the CVP (caudal vein plexus) in zebrafish. In control embryos, CVP were formed honeycomb-like structures at the tail around 48-hpf. In contrast, ADAMTS18 knock down resulted in specific defects in CVP formation. Notably, poor blood circulation in the CV (caudal vein) and CCV (common cardinal vein) was observed in ADAMTS18-e3i3-MO injected zebrafish compared to that of control zebrafish. To disclose the potential signaling molecules involved in vascular abnormities, the proteins extracted from common carotid artery (CCA) of WT and ADAMTS18 KO mice were analyzed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) analysis. A total of 510 proteins in CCA were identified, and 77 of these proteins (~15%) of ADAMTS18 KO mice were differentially expressed compared to WT mice. 22 of the 77 (~29%) proteins are responsible for the regulation of vascular morphology and angiogenesis. Ingenuity® Pathway Analysis (IPA) predicated that TGFβ signaling (z-score = 2.358) was significantly activated. The key molecules involved in TGFβ signaling were then examined by Western blotting. Compared to WT mice, the expression of ALK-1 (a type of TGFβ receptor I, TβRI), smad-1, -5, phosphorylated smad-1, -5 were significantly decreased in the carotid artery of ADAMTS18 KO mice, while the expression of ALK-5 (another type of TGF-β receptor I) smad-2, -3, phosphorylated smad-2, -3 were significantly increased, which may result in the reduced endothelial cell proliferation and migration in ADAMTS18 KO mice. Conclusions: These data imply crucial roles of ADAMTS18 in the regulation of angiogenesis in vivo. Disclosures No relevant conflicts of interest to declare.

Ces travaux de thèse démontrent que la protocadhérine-18a (Pcdh18a), exprimée par les progéniteurs des cellules stromales, joue un rôle important dans leur migration, puis dans la formation de la première niche d’hématopoïèse définitive, appelé tissu hématopoïétique caudal chez le poisson zèbre. La genèse des filopodes et la migration de cellules stromales, exprimant une Pcdh18a tronquée dans sa partie cytoplasmique (Pcdh18a-ΔCP106), sont compromises et les connexions cellulaires sont plus durables au cours de la migration. Cela suggère que le domaine cytoplasmique de Pcdh18a affecte la régulation de l’actine-F et est impliqué dans la médiation de la répulsion cellulaire. L’expression de Pcdh18a-ΔCP106 conduit aussi à une diminution du nombre de cellules stromales, et altère la formation du plexus veineux, composant majeur de la niche, résultant en une niche hématopoïétique non fonctionnelle. Elle induit également la surexpression de la fibronectine 1b, ce qui contribue probablement à la morphogenèse anormale du plexus veineux. Enfin, nous avons découvert qu'un motif à quatre acides aminés REDV présent dans la région extracellulaire de Pcdh18a est requis pour la fixation des cellules stromales sur les vaisseaux et leur différenciation en cellules stromales périvasculaires
This work demonstrates that protocadherin-18a (Pcdh18a), expressed by the stromal cell progenitors, plays important roles in their migration and the subsequent formation of the first niche of definitive hematopoiesis, called the caudal hematopoietic tissue in zebrafish. The genesis of filopodia and migration of stromal cells expressing a Pcdh18a, lacking a major part of its cytoplasmic domain (Pcdh18a-ΔCP106), are compromised and cellular connections are retained for a longer time during cell migration. These results suggest that the cytoplasmic domain of Pcdh18a affects F-actin regulation and is also involved in cell-contact-mediated repulsion. Expression of Pcdh18a-ΔCP106 also leads to a 2-fold decrease in the number of stromal cells, and alters the formation of the venous plexus, the other main component of the niche, resulting in a non-functioning hematopoietic niche. It also induces the overexpression of fibronectin 1b, which probably contributes to the abnormal morphogenesis of the venous plexus. Finally, we found that the four-amino-acid motif REDV present in the extracellular region of Pcdh18a appears required for the attachment of stromal cells onto the vessels and their differentiation in stromal perivascular cells