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Vascular Patterning (vascular + patterning)
Selected AbstractsThe Allantoic Core Domain: New insights into development of the murine allantois and its relation to the primitive streakDEVELOPMENTAL DYNAMICS, Issue 3 2009Karen M. Downs Abstract The whereabouts and properties of the posterior end of the primitive streak have not been identified in any species. In the mouse, the streak's posterior terminus is assumed to be confined to the embryonic compartment, and to give rise to the allantois, which links the embryo to its mother during pregnancy. In this study, we have refined our understanding of the biology of the murine posterior primitive streak and its relation to the allantois. Through a combination of immunostaining and morphology, we demonstrate that the primitive streak spans the posterior extraembryonic and embryonic regions at the onset of the neural plate stage (,7.0 days postcoitum, dpc). Several hours later, the allantoic bud emerges from the extraembryonic component of the primitive streak (XPS). Then, possibly in collaboration with overlying allantois-associated extraembryonic visceral endoderm, the XPS establishes a germinal center within the allantois, named here the Allantoic Core Domain (ACD). Microsurgical removal of the ACD beyond headfold (HF) stages resulted in the formation of allantoic regenerates that lacked the ACD and failed to elongate; nevertheless, vasculogenesis and vascular patterning proceeded. In situ and transplantation fate mapping demonstrated that, from HF stages onward, the ACD's progenitor pool contributed to the allantois exclusive of the proximal flanks. By contrast, the posterior intraembryonic primitive streak (IPS) provided the flanks. Grafting the ACD into TC/TC hosts, whose allantoises are significantly foreshortened, restored allantoic elongation. These results revealed that the ACD is essential for allantoic elongation, but the cues required for vascularization lie outside of it. On the basis of these and previous findings, we conclude that the posterior primitive streak of the mouse conceptus is far more complex than was previously believed. Our results provide new directives for addressing the origin and development of the umbilical cord, and establish a novel paradigm for investigating the fetal/placental relationship. Developmental Dynamics 238:532,553, 2009. © 2009 Wiley-Liss, Inc. [source] Glioblastoma cells incorporate into tumor vasculature and contribute to vascular radioresistanceINTERNATIONAL JOURNAL OF CANCER, Issue 9 2010Candice A. Shaifer Abstract Glioblastoma multiforme (GBM) remains the most devastating neoplasm of the central nervous system and has a dismal prognosis. Ionizing radiation represents an effective therapy for GBM, but radiotherapy remains only palliative because of radioresistance. In this study, we demonstrate that glioma cells participate in tumor vascularization and contribute to vascular radioresistance. Using a 3-dimensional coculture system, we observed an intimate interaction of glioma cells with endothelial cells whereby endothelial cells form vascular structures, followed by the recruitment and vascular patterning of glioma cells. In addition, tumor cells stabilize the vascular structures and render them radioresistant. Blocking initial endothelial vascular formation with endothelial-specific inhibitors prevented tumor cells from forming any structures. However, these inhibitors exhibited minimum effects on vascular structures formed by tumor cells, due to the absence of the targeted receptors on tumor cells. Consistent with the in vitro findings, we show that glioma cells form perfused blood vessels in xenograft tumor models. Together, these data suggest that glioma cells mimic endothelial cells and incorporate into tumor vasculature, which may contribute to radioresistance observed in GBM. Therefore, interventions aimed at the glioma vasculature should take into consideration the chimeric nature of the tumor vasculature. [source] Three-dimensional reconstruction of the remodeling of the systemic vasculature in early pig embryosMICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2008Pieter Cornillie Abstract Current research on angiogenesis and vascular regression is mainly focused on pathological conditions such as tumor growth and diabetic retinopathy, while a suitable physiological model to study the controlling factors in these processes is still lacking. The remodeling pattern of the embryonic vasculature into the adult configuration, such as the branchial arch arterial system developing into the aorta or the early embryonic veins building the caudal vena cava can potentially serve as a model. However, practical applications of the embryonic vascular patterning are impeded by the current controversy over the exact development of the caudal vena cava in mammals. To elucidate these ambiguities, specific developmental stages of vascular development in pig embryos were mapped by means of computer-assisted 3D reconstructions starting from histological serial sections of Bouin's fixed embryos. Special attention was given to venous segments in the lumbar region, as their origin and fate are equivocally described in literature. Here we demonstrate that these venous segments originate from the caudal cardinal veins which are forced to migrate during development into a more dorsal position due to the expansion of the developing metanephroi and the more dorsal relocation of the umbilical arteries. These findings are in contrast with the generally accepted theory that the venous segments in the lumbar region arise from newly formed veins that are located dorsal to the early caudal cardinal system. Microsc. Res. Tech., 2008. © 2007 Wiley-Liss, Inc. [source] Neurocan in the embryonic avian heart and vasculatureTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 2 2003Noboru Mishima Abstract The chondroitin sulfate proteoglycan (CSPG) neurocan was previously considered to be nervous-system specific. However, we have found neurocan in the embryonic heart and vasculature. In stage 11 quail embryos, neurocan was prominently expressed in the myocardium, dorsal mesocardium, heart-forming fields, splanchnic mesoderm, and vicinity of the extraembryonic vaculature, and at lower levels in the endocardium. A comparison of neurocan staining with QH1 staining of vascular endothelial cells demonstrates that neurocan is frequently expressed by cells adjacent to endothelial cells, rather than by endothelial cells themselves. In some cases, a dispersed subset of cells are neurocan-positive in a field of cells that otherwise appear uniform in morphology. Later in development, neurocan expression becomes relatively limited to the nervous system. However, even in 10-day embryos, neurocan is expressed in the chorio-allantoic membrane in the tissue that separates closely packed, small-diameter blood vessels. In summary, our results suggest that neurocan may function as a barrier that regulates vascular patterning during development. Anat Rec Part A 272A: 556,562, 2003. © 2003 Wiley-Liss, Inc. [source] STY1 regulates auxin homeostasis and affects apical,basal patterning of the Arabidopsis gynoeciumTHE PLANT JOURNAL, Issue 1 2006Joel J. Sohlberg Summary Gynoecia of the Arabidopsis mutant sty1-1 display abnormal style morphology and altered vascular patterning. These phenotypes, which are enhanced in the sty1-1 sty2-1 double mutant, suggest that auxin homeostasis or signalling might be affected by mutations in STY1 and STY2, both members of the SHI gene family. Chemical inhibition of polar auxin transport (PAT) severely affects the apical,basal patterning of the gynoecium, as do mutations in the auxin transport/signalling genes PIN1, PID and ETT. Here we show that the apical,basal patterning of sty1-1 and sty1-1 sty2-1 gynoecia is hypersensitive to reductions in PAT, and that sty1-1 enhances the PAT inhibition-like phenotypes of pin1-5, pid-8 and ett-1 gynoecia. Furthermore, we show that STY1 activates transcription of the flavin monooxygenase-encoding gene THREAD/YUCCA4, involved in auxin biosynthesis, and that changes in expression of STY1 and related genes lead to altered auxin homeostasis. Our results suggest that STY1 and related genes promote normal development of the style and affect apical,basal patterning of the gynoecium through regulation of auxin homeostasis. [source] 4145: Analysis of mouse eye mutants as models for human diseasesACTA OPHTHALMOLOGICA, Issue 2010S JADEJA Purpose The Eumodic (European Mouse Disease Clinic) project screens mouse knockout lines and ENU induced mutants for pathological phenotypes. Initially 2 of the strains identified with an eye defect by the Sanger MGP and a strain from the ENU mutagenesis screen at MRC Harwell have been selected for further investigation. Methods Following the initial primary phenotyping, pathology; histology; and immunohistochemistry was carried out on ocular tissue collected from mutant and control animals to determine defects in eye structure and development. This gave an indication to the underlying cause of the defects seen, enabling further molecular biology analysis. Results Btb/Poz Domain-containing Protein 12 (Btbd12) is a scaffold protein required for the formation of DNA repair complexes. The mouse knockout of this gene shows corneal opacity, dilated pupils and occasional microphthalmia, modelling the phenotypes seen in human diseases of defective DNA repair. The corneas of the mutant animals exhibit increased DNA damage which is likely to be the cause of the opacification. Solute Carrier Family 9 Member 8 (Slc9a8) is a Sodium/ Hydrogen exchanger and has previously been shown to play a role in ion exchange. The Slc9a8 knockout strain appears to have retinal degeneration and the males are infertile. The ENU-induced mutant Pedv128 exhibits defects in the retinal vasculature including defective vascular patterning and increased vascular leakage. Of particular interest is that this vascular phenotype is restricted to the eyes. Conclusion Investigation of mouse eye mutants can result in a better understanding of the pathology and underlying causes of human diseases. [source] | |||||||||||||