ライフサイエンスコーパス: angioblast

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

20 Angioblasts aligned forming cords before morphologically

21 ration and proper spatial arrangement of the angioblasts allow subsequent assembly of vascular tubes.

22 ve very useful in studying commitment to the angioblast and beyond.

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

26 phosphate dehydrogenase (M-a-GPDH) (to label angioblasts and developing blood vessels).

27 uted to it promoting migratory activities of angioblasts and early endothelial cells required for the

28 Increased angioblasts and EC numbers in GT of ECIRS1 mice were due

29 ision and p-eNOS((S1177)) expression in both angioblasts and embryonic endothelial cells (EECs, TAL-1

30 the visceral yolk sac and later in embryonic angioblasts and endocardium.

31 ulating chemoattraction and proliferation of angioblasts and endothelial cells and that VEGF-A expres

32 oliferation and accumulation of disorganized angioblasts and endothelial cells around the lens.

33 Coexpression of CD39 (marker for retinal angioblasts and endothelial cells) and CXCR4 or c-Kit wa

34 Previously we showed that periocular angioblasts and forming ocular blood vessels avoid the p

35 Zebrafish ecscr is expressed in angioblasts and in axial vessels during angioblast migra

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

41 uggesting that this cell population includes angioblasts and their progenitors.

42 oposed to serve as a chemoattractant for the angioblasts and to regulate this medial migration.

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

49 The angioblasts are capable of differentiating into RBCs via

50 in which the PGCs, allantois primordium, and angioblasts are first detected.

51 Angioblasts are multipotent progenitor cells that give r

52 Angioblasts are precursor cells of the vascular endothel

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

55 Although competent Cxcr4-positive angioblasts are present on the right, they fail to form

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

58 To determine how angioblasts assemble into cranial vasculature, we genera

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

63 and a compensatory increase in the number of angioblast cells in the same trunk region.

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.

66 Such angioblast cluster-derived angiogenesis is likely to be

67 anial vessels originate by angiogenesis from angioblast clusters, which themselves form by the mechan

68 Individual angioblasts coalesce to form the primary vascular plexus

69 In this study, we analyze mechanisms of angioblast coalescence in the zebrafish embryonic midlin

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

74 Angioblasts deficient in Hh signaling fail to contribute

75 , and resulted in a striking augmentation of angioblast-dependent neovascularization.

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.

79 Individual angioblasts destined for the ISVs arise from the lateral

80 t the top of the known genetic hierarchy for angioblast development.

81 nrk-1, which also plays a functional role in angioblast development.

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

84 Importantly, vasculogenesis and angioblast differentiation steps were unaffected in syx

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.

90 This study was designed to test whether such angioblasts exist in neonatal mouse retina.

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.

93 Rasipl null angioblasts fail to properly localize the polarity deter

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

96 In kus(tr12) mutants, angioblast formation and initial sprouting are normal, b

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

99 Endothelial cell progenitors, angioblasts, have been detected in the peripheral blood

100 Progeny of each angioblast, however, are restricted to one of the vessel

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

104 ts that signals from the notochord may guide angioblasts in the fashioning of the dorsal aorta.

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

107 rom clusters of extraembryonic and embryonic angioblasts in the murine conceptus.

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 migration, specification, and arrangement of angioblasts into arterial and venous lineages, a process

113 Sema3A inhibitor causes ectopic migration of angioblasts into the cornea and results in its subsequen

114 spatially with the early differentiation of angioblasts into the endothelial cell lineage and the pr

115 helial growth factor (VEGF), known to affect angioblast invasion and myocardial proliferation and sur

116 w lower amounts of active Cdc42 and Rac1 and angioblasts isolated from these knockdown embryos search

117 both survival and proliferation of allantoic angioblasts, it was not sufficient to induce appropriate

118 VEGFR)-2 (a marker for endothelial cells and angioblasts) labeled the vascular network but failed to

119 thodology for indirect lineage conversion to angioblast-like cells adds to the armamentarium of repro

120 Although specification of the angioblast lineage is independent of endoderm interactio

121 We find that angioblasts migrate as individual cells to form a vascul

122 ion, but that during subsequent development, angioblasts migrate from the lateral plate mesoderm to t

123 To form the first axial vessels, angioblasts migrate towards the midline and coalesce und

124 tances from the graft, indicating that mouse angioblasts migrated extensively in avian hosts.

125 (Sema3A), a cell guidance chemorepellent, on angioblast migration and corneal avascularity during dev

126 wn about what controls the precise timing of angioblast migration and their final destination at the

127 wever, the molecular mechanisms that prevent angioblast migration and vascularization of the developi

128 d in angioblasts and in axial vessels during angioblast migration and vasculogenesis.

129 We further show that during this angioblast migration Apelin receptor signaling is mainly

130 rected ecscr knockdown resulted in defective angioblast migration in the posterior lateral plate meso

131 anterior to posterior progression of midline angioblast migration is facilitated by retinoic acid-ind

132 Using zebrafish, we found that midline angioblast migration requires neighboring tissue rearran

133 ave previously been implicated in regulating angioblast migration, we hereby provide a novel mechanis

134 sues to facilitate notochord positioning and angioblast migration, which is ultimately responsible fo

135 In vertebrates, molecular mechanisms dictate angioblasts' migration and subsequent differentiation in

136 of endocardial precursor cells (endocardial angioblasts) occurred within the precardiac mesoderm and

137 t evidence suggests that bone marrow-derived angioblasts or endothelial progenitor cells circulate in

138 Together, Dusp-5 and Snrk-1 control angioblast populations in the lateral plate mesoderm wit

139 uctive events, involving the mesenchymal and angioblast populations, whereby Wt1-stimulated expressio

140 lineage tracking in zebrafish embryos, that angioblast precursors for the trunk artery and vein are

141 d PECAM, Rasip1 is specifically expressed in angioblasts prior to vessel formation, in the initial em

142 rculation, following de novo aggregation of "angioblast" progenitors in a process called vasculogenes

143 enge this model and instead demonstrate that angioblasts rely on their intrinsic expression of Apelin

144 plexus originate from a pool of specialized angioblasts residing in the floor of the posterior cardi

145 hing of the ureteric bud, the Flk1-dependent angioblast signal is no longer required to maintain bran

146 eceptor-expressing, developmentally arrested angioblasts simultaneously coexpress Epo, which may repr

147 onal events that induce etsrp expression and angioblast specification are not well understood.

148 on factors critical for etsrp expression and angioblast specification from mesoderm.

149 he adjacent endoderm are necessary to induce angioblast specification within the mesoderm.

150 e conclude that endoderm is not required for angioblast specification, but does play an essential rol

151 While scl was not required for angioblast specification, forced expression of exogenous

152 elial cells are developmentally derived from angioblasts specified in the mesodermal germ cell layer.

153 ((T495)) was expressed in a subpopulation of angioblasts (TAL-1(+)/Flk-1(+)/CD31(-)/CD34(-)/VE-Cadher

154 ors are composed of developmentally arrested angioblasts that coexpress erythropoietin (Epo) and Epo

155 e signaling by hepatic stellate cells and/or angioblasts that coisolate with them.

156 Angioblasts that form the major axial blood vessels of t

157 Thus, MM cells resemble early renal angioblasts that may provide an ideal platform for the i

158 However, within angioblasts the precise biochemical signals that determi

159 Angioblasts, the precursor cells that comprise the endot

160 bryos lacking endoderm contain aggregates of angioblasts, these angioblasts fail to assemble into end

161 ping retinal vessels and was not observed in angioblasts throughout normal postnatal development.

162 a signal from the endoderm is necessary for angioblasts to assemble into a vascular network and to u

163 o plays a cell-autonomous role in specifying angioblasts to become arterial cells, and Hh signaling-d

164 lycemia per se does not alter the ability of angioblasts to differentiate or of angioblast-derived en

165 ing in GT to decrease the differentiation of angioblasts to EC, which was normalized by enhancing ins

166 in the trunk by migration and coalescence of angioblasts to form endothelial tubes.

167 These include aggregation of angioblasts to form the primitive vascular plexus, follo

168 avity that provides a physical space for the angioblasts to migrate into.

169 the migration of endothelial precursors, the angioblasts, to the position of the future vessels.

170 Our results argue that the medial angioblasts undergo arterial differentiation because the

171 nsgenic reporters, we demonstrate that these angioblasts undergo two phases of migration and differen

172 kt and EC numbers by >50% without changes in angioblasts versus WT mice, which were improved in ECIRS

173 of the trunk and limb, marked somite-derived angioblasts were followed in developing embryos.

174 utative endothelial cell (EC) progenitors or angioblasts were isolated from human peripheral blood by

175 Fetal liver kinase (Flk1)-positive angioblasts were significantly decreased in T(C)/T(C) al

176 rter transgene (Tg(lmo2:EGFP)), we show that angioblasts were specified normally in the absence of sc

177 he assembly of endothelial precursors called angioblasts, whereas in angiogenesis new vessels arise b

178 ve Flt-1 and Flk-1 were observed in isolated angioblasts, whereas VEGF was not detected.

179 icits an as-yet-unidentified signal from the angioblasts, which is required to stimulate the expressi

180 From this pool emerges angioblasts, which migrate anteriorly into the nerve fib

181 Feeders of angioblasts yielded self-replication, stellate cell prec