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1 nd not vasculogenesis (assembly of dispersed angioblasts).
2 are alleged to be vascular precursor cells (angioblasts).
3 n the process of mesoderm specification into angioblast.
4 l human bone marrow (BM) is a progenitor for angioblasts.
5 lls - a phenotype that would be expected for angioblasts.
6 doderm is not necessary for the induction of angioblasts.
7 is not required for the initial formation of angioblasts.
8 vessels are recognized by mammalian somitic angioblasts.
9 ggest that they are derived from circulating angioblasts.
10 hat TAL1/SCL-positive/QH1-negative cells are angioblasts.
11 ly that clo fails to differentiate blood and angioblasts.
12 pressing cells and therefore appears to lack angioblasts.
13 n of Vegf and Hh morphogens than the lateral angioblasts.
14 b as a direct upstream regulator of etsrp in angioblasts.
15 gration, maintenance, and differentiation of angioblasts.
16 ntenance, but not for the differentiation of angioblasts.
17 y immunoselection technologies, included (1) angioblasts, (2) mature endothelia, (3) hepatic stellate
18 endothelial cells and thus can be defined as angioblasts; (2) hematopoietic cells of blood islands ex
19 of Notch receptor expression in dorsal aorta angioblasts, activation of Notch signaling in hey2 morph
21 ration and proper spatial arrangement of the angioblasts allow subsequent assembly of vascular tubes.
23 ed eNOS phosphorylation on Ser1177 regulates angioblast and EEC division, which underlies the formati
24 a reduction in p-eNOS((S1177)) expression in angioblast and EECs that is correlated with a decrease i
25 e to impaired migration and proliferation of angioblasts and arterial endothelial cells while not aff
27 uted to it promoting migratory activities of angioblasts and early endothelial cells required for the
29 ision and p-eNOS((S1177)) expression in both angioblasts and embryonic endothelial cells (EECs, TAL-1
31 ulating chemoattraction and proliferation of angioblasts and endothelial cells and that VEGF-A expres
33 Coexpression of CD39 (marker for retinal angioblasts and endothelial cells) and CXCR4 or c-Kit wa
36 have determined that dusp-5 is expressed in angioblasts and in established vasculature and that it c
37 events that regulate the differentiation of angioblasts and mature endothelial cells from their meso
38 n of blood vessels from mesodermally derived angioblasts and the incorporation and differentiation of
39 , the differentiation of mesodermal cells to angioblasts and the subsequent formation of blood island
40 e differentiation of retinal precursors into angioblasts and their migration to sites of vessel assem
43 n Nrp1(Sema-) mutant mice results in ectopic angioblasts and vascularization of the embryonic mouse c
44 ansion, suggesting that aberrant division of angioblasts and/or endothelial cells is a hallmark of th
45 ewborn mice contain endothelial progenitors (angioblasts) and that when embryonic day 12 kidneys are
46 ositive population, including Flk-1-positive angioblasts, and accelerates kidney development in vitro
47 cells that developed from migratory somitic angioblasts, and assembly of these vessels is likely to
48 ) transplants consistently produced invasive angioblasts, and contributed to the lateral rectus and p
53 We find that, initially, no flk-1-expressing angioblasts are present at this location, but that durin
54 Prior investigation has demonstrated that angioblasts are present in the inner retinas of human em
56 ind that during normal development the first angioblasts arise laterally in the mesoderm and then mig
57 key role in controlling the amplification of angioblasts as well as their differentiation into endoth
59 d that VEGF can act as a chemoattractant for angioblasts by ectopic expression of VEGF in the embryo.
60 e that ecscr promotes migration of zebrafish angioblasts by enhancing endothelial kdr sensitivity to
61 ells and an accompanying accumulation of the angioblast cell population that was associated with diso
62 To investigate the mechanisms that initiate angioblast cell transcription during embryogenesis, we h
64 The results showed that MM cells possess angioblast characteristics by expressing phenotypic mark
65 ial-venous differentiation that explains how angioblasts choose between an arterial and venous fate.
67 anial vessels originate by angiogenesis from angioblast clusters, which themselves form by the mechan
70 y, our findings suggest that PCV-specialized angioblasts contribute not only to the formation of the
71 Rasip1-deficient vessels transition from an angioblast cord to a hollow tube, permit circulation of
72 D34(+) cells) that appear to be enriched for angioblasts could be used to accelerate the rate of bloo
73 F receptor activity in zebrafish resulted in angioblast deficiencies that partially overlap with thos
76 patterning cues are recognized by mammalian angioblasts derived from somitic mesoderm through analys
77 nhance angioblast differentiation but impair angioblast-derived endothelial cell survival or prolifer
78 bility of angioblasts to differentiate or of angioblast-derived endothelial cells to proliferate.
82 me arterial cells, and Hh signaling-depleted angioblasts differentiate into venous cells instead.
83 In contrast, hyperinsulinemia may enhance angioblast differentiation but impair angioblast-derived
85 ysis at the cellular level showed defects in angioblast differentiation to endothelial cells and an a
86 aling pathway, while affecting the number of angioblasts, does not appear to affect their migratory b
87 h the aggregation and subsequent assembly of angioblasts (endothelial precursors) into a network of e
88 cell-autonomous mechanism of Hh signaling in angioblasts (endothelial progenitor cells) during arteri
89 l how vascular endothelial progenitor cells (angioblasts) establish their arterial or venous fates.
91 d with kidney vascularization and identified angioblasts expressing Flt-1 and Flk-1 in prevascular em
92 erm contain aggregates of angioblasts, these angioblasts fail to assemble into endothelial tubes.
94 ers of endothelial cells (Flk1(+)/PECAM(+)), angioblasts (Flk1(+)/PECAM(-)), or undifferentiated meso
95 bilized autologous human bone-marrow-derived angioblasts for revascularization of infarcted myocardiu
97 pose of this study was to characterize these angioblasts further and examine ligands that might contr
98 ic structures with little or no capacity for angioblast generation act as a nexus for vessel patterni
101 ression of HoxB5 led to expansion of flk1(+) angioblasts in differentiating embryoid bodies and incre
102 rmore, animal caps stimulated with bFGF form angioblasts in the absence of any detectable endodermal
103 mation of blood islands and blood vessels by angioblasts in the conceptus, is a dynamic process modul
105 al aortic arch first appears as an island of angioblasts in the lateral pharyngeal mesoderm, then ela
106 om clusters of extra-embryonic and embryonic angioblasts in the murine conceptus using both in vitro
108 as associated with forming blood vessels and angioblasts in the nerve fiber layer (NFL) of peripheral
109 cell-tracker DiI showed that somite-derived angioblasts in unperturbed embryos migrated extensively
110 tional cell types--such as stromal cells and angioblasts--in growth and patterning of the nephron.
111 e marrow-derived endothelial progenitors, or angioblasts, induce neovascularization of infarcted myoc
112 Sema3A inhibitor causes ectopic migration of angioblasts into the cornea and results in its subsequen
113 spatially with the early differentiation of angioblasts into the endothelial cell lineage and the pr
114 helial growth factor (VEGF), known to affect angioblast invasion and myocardial proliferation and sur
115 w lower amounts of active Cdc42 and Rac1 and angioblasts isolated from these knockdown embryos search
116 both survival and proliferation of allantoic angioblasts, it was not sufficient to induce appropriate
117 VEGFR)-2 (a marker for endothelial cells and angioblasts) labeled the vascular network but failed to
118 thodology for indirect lineage conversion to angioblast-like cells adds to the armamentarium of repro
121 ion, but that during subsequent development, angioblasts migrate from the lateral plate mesoderm to t
124 (Sema3A), a cell guidance chemorepellent, on angioblast migration and corneal avascularity during dev
125 wever, the molecular mechanisms that prevent angioblast migration and vascularization of the developi
128 rected ecscr knockdown resulted in defective angioblast migration in the posterior lateral plate meso
129 ave previously been implicated in regulating angioblast migration, we hereby provide a novel mechanis
130 In vertebrates, molecular mechanisms dictate angioblasts' migration and subsequent differentiation in
131 of endocardial precursor cells (endocardial angioblasts) occurred within the precardiac mesoderm and
132 t evidence suggests that bone marrow-derived angioblasts or endothelial progenitor cells circulate in
134 uctive events, involving the mesenchymal and angioblast populations, whereby Wt1-stimulated expressio
135 lineage tracking in zebrafish embryos, that angioblast precursors for the trunk artery and vein are
136 d PECAM, Rasip1 is specifically expressed in angioblasts prior to vessel formation, in the initial em
137 rculation, following de novo aggregation of "angioblast" progenitors in a process called vasculogenes
138 enge this model and instead demonstrate that angioblasts rely on their intrinsic expression of Apelin
139 plexus originate from a pool of specialized angioblasts residing in the floor of the posterior cardi
140 hing of the ureteric bud, the Flk1-dependent angioblast signal is no longer required to maintain bran
141 eceptor-expressing, developmentally arrested angioblasts simultaneously coexpress Epo, which may repr
145 e conclude that endoderm is not required for angioblast specification, but does play an essential rol
147 elial cells are developmentally derived from angioblasts specified in the mesodermal germ cell layer.
148 ((T495)) was expressed in a subpopulation of angioblasts (TAL-1(+)/Flk-1(+)/CD31(-)/CD34(-)/VE-Cadher
149 ors are composed of developmentally arrested angioblasts that coexpress erythropoietin (Epo) and Epo
154 bryos lacking endoderm contain aggregates of angioblasts, these angioblasts fail to assemble into end
155 ping retinal vessels and was not observed in angioblasts throughout normal postnatal development.
156 a signal from the endoderm is necessary for angioblasts to assemble into a vascular network and to u
157 o plays a cell-autonomous role in specifying angioblasts to become arterial cells, and Hh signaling-d
158 lycemia per se does not alter the ability of angioblasts to differentiate or of angioblast-derived en
159 ing in GT to decrease the differentiation of angioblasts to EC, which was normalized by enhancing ins
162 the migration of endothelial precursors, the angioblasts, to the position of the future vessels.
164 nsgenic reporters, we demonstrate that these angioblasts undergo two phases of migration and differen
165 kt and EC numbers by >50% without changes in angioblasts versus WT mice, which were improved in ECIRS
167 utative endothelial cell (EC) progenitors or angioblasts were isolated from human peripheral blood by
169 rter transgene (Tg(lmo2:EGFP)), we show that angioblasts were specified normally in the absence of sc
170 he assembly of endothelial precursors called angioblasts, whereas in angiogenesis new vessels arise b
172 icits an as-yet-unidentified signal from the angioblasts, which is required to stimulate the expressi
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