ライフサイエンスコーパス: yolk sac

1 isceral endoderm defects observed in the cKO yolk sac.

2 important role in the proper development of yolk sac.

3 y in trophoblast giant cells in the parietal yolk sac.

4 omic data for the coelomic fluid bathing the yolk sac.

5 especially apparent in small vessels of the yolk sac.

6 n vessel remodeling in the developing murine yolk sac.

7 to induce vessel remodeling in the mammalian yolk sac.

8 s and emerge within the blood islands of the yolk sac.

9 and vasculogenesis were normal in embryo and yolk sac.

10 eloping vasculature of the embryo proper and yolk sac.

11 n and/or stability of erythroid cells in the yolk sac.

12 second wave of HSCs begins to emerge in the yolk sac.

13 he placenta, and the epithelial cells of the yolk sac.

14 lood vessel formation in the embryo body and yolk sac.

15 om Mesp1-Cre(+) cells in both the embryo and yolk sac.

16 Predominant histology was yolk sac.

17 m which is derived the embryo proper and the yolk sac.

18 n both the labyrinth of the placenta and the yolk sac.

19 ickettsiae isolated from embryonated hen egg yolk sacs.

20 Indian Hedgehog are reduced in chato mutant yolk sacs.

21 endothelial Rac1-deficient embryos and their yolk sacs.

22 cripts, whereas there were few changes in KO yolk sacs.

23 to defective erythropoiesis in Hif1alpha-/- yolk sacs.

24 were reduced by approximately 80% in Klf6-/- yolk sacs.

25 hen the blastoderm begins to spread over the yolk sac, a process involving coordinated epithelial sur

26 it is physiologically expressed in the fetal yolk sac, a tissue derived from the extraembryonic endod

27 In embryos, all blood cells within the yolk sac and aorta were of Flk-1(+) origin.

28 of specific myeloid cell progenitors of both yolk sac and bone marrow origin.

29 rom erythromyeloid progenitors (EMPs) in the yolk sac and develop in the forming CNS.

30 eover, those cells are not released from the yolk sac and disseminated into embryonic tissues.

31 of several embryonic regions, including the yolk sac and dorsal aorta, that undergoes vasculogenesis

32 cted proliferative capacity persist in E10.5 yolk sac and E11.5 liver.

33 microscopy has advanced our understanding of yolk sac and early embryonic vascularization.

34 In null mice, vessels throughout the yolk sac and embryo form and recruit smooth muscle in a

35 ulatory differences in Epo/EpoR signaling in yolk sac and embryonic erythropoiesis.

36 round midgestation, when connections between yolk sac and embryonic vasculature mature.

37 CNS, originate during embryogenesis from the yolk sac and enter the CNS quite early (embryonic day 9.

38 ryocyte progenitors begins to decline in the yolk sac and expand in the fetal liver.

39 ion of cancer cells after injection into the yolk sac and extravasation of cancer cells into tissues

40 eration of a unique, previously unrecognized yolk sac and fetal liver progenitor, which we propose ac

41 rimitive erythroid lineage originates in the yolk sac and generates a cohort of large erythroblasts t

42 ell type was present abundantly in the early yolk sac and in fewer numbers (approximately 5% of that

43 sful establishment of nascent vasculature in yolk sac and in the developing embryos.

44 VE-PTP-null mice were most pronounced in the yolk sac and include a complete failure to elaborate the

45 yonic (E9) B-cell progenitors located in the yolk sac and intraembryonic hemogenic endothelium before

46 auses midgestation lethality, with defective yolk sac and intraembryonic vasculature.

47 Parietal endoderm (PE) contributes to the yolk sac and is the first migratory cell type in the mam

48 mergence of definitive erythropoiesis in the yolk sac and its transition to the fetal liver.

49 d extraembryonic ectoderm, as well as in the yolk sac and labyrinth tissues that form later.

50 types in normal embryos, as well as in E13.5 yolk sac and labyrinth.

51 ineage tracing revealed that the majority of yolk sac and many adult hematopoietic cells derive from

52 nd visualized at embryonic day (E)9.0 in the yolk sac and neuroectoderm; 2) at E10.5, CX3CR1 single-p

53 ainly from progenitor cells generated in the yolk sac and of 'passenger' or 'transitory' myeloid cell

54 rrent with reduced erythrocyte velocity, and yolk sac and pericardium oedema.

55 Yolk sac and placenta are required to sustain embryonic

56 s and is expressed in the visceral endoderm, yolk sac and placenta.

57 the aorta, vitelline and umbilical arteries, yolk sac and placenta.

58 ession of one or more imprinted genes in the yolk sac and placenta.

59 delete YY1 from the visceral endoderm of the yolk sac and the definitive endoderm of the embryo.

60 extensive arterial morphogenesis both in the yolk sac and the embryo proper and disrupted arterial-ve

61 ath had markedly deformed vasculature of the yolk sac and the embryo, as well as poorly looped hearts

62 revealed abnormalities in both the visceral yolk sac and the embryo, including stunted extraembryoni

63 We demonstrate that DPFCs originate in the yolk sac and then rapidly migrate to other extra- and in

64 nd defects in iron homeostasis, Hif1alpha-/- yolk sac and/or embryos demonstrated aberrant mRNA level

65 genitor cells (HSCs/Ps) originating from the yolk sac and/or para-aorta-splanchno-pleura/aorta-gonad-

66 cing (RNA-seq) data for the human and murine yolk sacs and compare those data with data for the chick

67 Further analysis of yolk sacs and embryos revealed a significant reduction o

68 The defects in Osr1-null yolk sacs and embryos were virtually identical to those

69 Aggf1+/- KO caused defective angiogenesis in yolk sacs and embryos.

70 nt, have aberrant vasculogenesis in embryos, yolk sacs and placentas, and die between embryonic day 1

71 It is found in yolk sacs and the outer cells of pre-implantation mouse

72 Genetic fate mapping revealed that yolk-sac and fetal monocyte progenitors gave rise to the

73 r developing structures, such as the kidney, yolk sac, and choroid plexus, suggests a possible genera

74 n leads to vascular defects in the placenta, yolk sac, and embryo proper, as well as abnormal neural

75 with profound vascular defects in placenta, yolk sac, and embryo proper, whereas heterozygous deleti

76 o found in other embryonic niches (placenta, yolk sac, and extraembryonic vessels), attempts to detec

77 etal liver, dorsal aorta, vitelline vessels, yolk sac, and heart.

78 cal order of large and small branches in the yolk sac, and impaired development of anterior cardinal

79 ood islands, the equivalent of the mammalian yolk sac, and migrate out to colonize the embryo.

80 ed to defective angiogenesis in the embryos, yolk sac, and placenta, impaired vasculature and associa

81 lex homolog), transfers IgY across the avian yolk sac, and represents a new class of Fc receptor rela

82 ascular abnormalities in the lung, placenta, yolk sac, and retina.

83 ion of target transcripts in placenta and/or yolk sac, and that some of these would be important for

84 roscopic analyses of E9.5 EKLF(-/-)KLF2(-/-) yolk sacs, and cytospins, indicate that erythroid and en

85 ected in R. prowazekii purified from hen egg yolk sacs, and G3PDH activity was assayable in R. prowaz

86 uclear envelope protein in the regulation of yolk-sac angiogenesis by TGFbeta signaling and reveal th

87 evelop adjacent to blood vessel walls in the yolk sac, aorta-gonad-mesonephros region, embryonic live

88 bryo and fetus: para-aortic splanchnopleura, yolk sac, aorta-gonad-mesonephros, liver, and bone marro

89 hematopoietic repopulating cells from murine yolk sac, aorta-gonad-mesonephros, placenta, fetal liver

90 at targets of miRNAs highly expressed in the yolk sac are significantly derepressed in GW182(gt/gt) m

91 Our results support the contribution of the yolk sac as a source of microglial precursors.

92 evels of Epo receptor (EpoR) in Hif1alpha-/- yolk sac as well as Epo and EpoR mRNA in Hif1alpha-/- em

93 alysis, we identified 2 waves of MEPs in the yolk sac associated with the primitive and definitive er

94 ells in the conceptus were identified in the yolk sac at E9.5, while large, highly reticulated platel

95 EMPs develop in the yolk sac at embryonic day (E) 8.5, migrate and colonize

96 erythroid colonies from HIF-1alpha-deficient yolk sacs at E9.5.

97 otential in vitro have been described in the yolk sac before emergence of HSCs, and fetal macrophages

98 d/myeloid progenitors [EMPs]) emerges in the yolk sac beginning at embryonic day 8.25 (E8.25) and col

99 the hemangioblast as the cell of origin for yolk sac blood and endothelium.

100 f-renewal in adults and also participates in yolk sac blood island formation.

101 In most vertebrates, yolk sac blood islands are the initial sites of appearan

102 Primitive hematopoiesis occurs in the yolk sac blood islands during vertebrate embryogenesis,

103 there is a marked absence of erythrocytes in yolk sac blood islands.

104 ied this method to the analysis of embryonic yolk sac blood islands.

105 transgenic mouse line led to a disruption in yolk sac blood vessel development.

106 ascular deletion of Brg1 results in aberrant yolk sac blood vessel morphology, which is rescued by ph

107 tic activity in mammalian development is the yolk-sac blood island, which originates from the hemangi

108 which will form the endoderm of the visceral yolk sac, BMP4-treated XEN cells regulated hematopoiesis

109 ut the same in both WT and KO mouse visceral yolk sac, brain, and spinal column.

110 or erythro-myeloid progenitors (EMPs) in the yolk sac, but it decreased the expression of alpha4-inte

111 mma-globin was co-expressed in the embryonic yolk sac, but not in the fetal liver; and wild-type beta

112 They appear in the yolk sac by embryonic day 7.5, begin to enter the embryo

113 sites of embryonic hematopoiesis such as the yolk sac by way of blood flow.

114 istration of synthetic TB4 partially rescues yolk sac capillary plexus formation in Hand1-null embryo

115 ion, bi-laminar disc formation, amniotic and yolk sac cavitation, and trophoblast diversification.

116 asts, LIM-3 was expressed neither in primary yolk sac cells transformed by unfused v-Myb nor in BM2 c

117 d Gpx3 in the same vesicles of d-13 visceral yolk sac cells, suggesting uptake by pinocytosis.

118 This study demonstrates that later yolk-sac Chinook larvae (before exogenous feeding) are e

119 not zeta-globin gene expression in the E10.5 yolk sac, compared with wild-type mice.

120 In differentiating mouse ES cells and mouse yolk sac cultures, addition of Indian Hh ligand increase

121 1-knock-out mice: no mature large vessels in yolk sacs, defective angiogenesis in the brain and inter

122 cKO embryos display profound yolk sac defects at 9.5 days post coitum (dpc), includin

123 ood of embryonic day (E) 10.5 embryos, while yolk sac definitive hematopoiesis was quantitatively nor

124 loblastic nucleated erythroblasts resembling yolk sac-derived cells.

125 Functionally, yolk sac-derived chemokine (C-C motif) receptor 2(-) mac

126 Significantly, E9.5 yolk sac-derived EMPs cultured in vitro have similar mur

127 We conclude that yolk sac-derived EMPs, the first of 2 origins of definit

128 in vitro but were rather supported on mouse yolk sac-derived endothelial cell (C166) feeder layers.

129 ctor Runx1 is essential for the formation of yolk sac-derived erythroid/myeloid progenitors (EMPs) an

130 with different ontogenetic origins: prenatal yolk sac-derived Kupffer cells and peripheral blood mono

131 , red pulp macrophages, a discrete subset of yolk sac-derived macrophages, were found to be altered i

132 irculating adult monocytes or from primitive yolk sac-derived macrophages.

133 Previously, we determined that yolk sac-derived primitive erythroblasts mature in the b

134 The recent paradigm shift that microglia are yolk sac-derived, not hematopoietic-derived, is reshapin

135 Furthermore, failure of yolk sac development or function is consistent with the

136 e hematopoiesis in a manner resembling human yolk sac development, thus providing a valuable tool for

137 roglia in the brain that originates from the yolk sac during early development.

138 increase in the incidence of pericardial and yolk sac edema relative to controls.

139 n dilbit WAF-exposed embryonic zebrafish but yolk sac edema was similar in all exposures.

140 of toxicity included pericardial, ocular and yolk sac edema, nondepleted yolk, spinal curvature, tail

141 erm cell tumor predominantly consisting of a yolk sac element (Fig 1).

142 Required histology included yolk sac, embryonal carcinoma, or choriocarcinoma.

143 hroid cells does not faithfully mimic either yolk sac embryonic or their fetal liver counterparts.

144 identify, in the fetal liver, a sequence of yolk sac EMP-derived and HSC-derived haematopoiesis, and

145 and HSC-derived haematopoiesis, and identify yolk sac EMPs as a common origin for tissue macrophages.

146 wn as GW182, is selectively expressed in the yolk sac endoderm and that gene trap disruption of GW182

147 Moreover, the Snx13-null visceral yolk sac endoderm cells showed dramatic changes in the o

148 in trophoblast lineages of the placenta and yolk sac endoderm, which occurs only from the maternally

149 iR-17/20/93/106 clusters highly expressed in yolk sac endoderm.

150 erize an ontogenic process of blood cell and yolk sac endothelial maturation that is required to disp

151 tivated a cardiac transcriptional program in yolk sac endothelium, leading to the emergence of CD31+P

152 After exiting the yolk sac, EryP begin to express cell adhesion proteins,

153 cells that develop during organogenesis from yolk-sac erythro-myeloid progenitors (EMPs) distinct fro

154 tissue-resident macrophages are derived from yolk sac erythromyeloid progenitors and fetal liver prog

155 t with ruffling of the neural fold ridges, a yolk sac erythropoietic failure, and elevated alpha-keto

156 ne-restricted potential originating from the yolk sac even before the emergence of the first hematopo

157 ved during primitive hematopoiesis in murine yolk sac explant cultures and embryonic stem cell assays

158 xtensively self-renew and can be seeded from yolk sac/foetal liver progenitors with little input from

159 Yolk sacs from embryonic day 11.5 (E11.5) Zfp36l2 KO mic

160 i, the exocoelomic cavity, and the secondary yolk sac function together as a physiological equivalent

161 OX7 is broadly expressed across the RUNX1(+) yolk sac HE population compared with SOX17.

162 ly well studied, the molecular regulation of yolk sac HE remains poorly understood.

163 We modeled T21 yolk sac hematopoiesis using human induced pluripotent s

164 specification in the dorsal aorta, enhanced yolk sac hematopoiesis, and exuberant cardiac blood isla

165 We show that the previously reported lack of yolk-sac hematopoiesis and vascular development in Ldb1(

166 nadal macrophages are derived from primitive yolk-sac hematopoietic progenitors and exhibit hallmarks

167 We found that the formation of yolk sac hemogenic endothelium and its hematopoietic pot

168 onal states characteristic of the definitive yolk sac, HSCs undergoing specification, and definitive

169 The chicken yolk sac IgY receptor (FcRY) is the ortholog of the mamm

170 ted remarkable proliferative capacity in the yolk sac immediately before the onset of circulation, wh

171 wer numbers (approximately 5% of that in the yolk sac) in the caudal half of the developing embryos.

172 In the absence of Eng, yolk sacs inappropriately express the cardiac marker, Nk

173 topoietic ontogeny reminiscent of the murine yolk sac, including overlapping waves of hemangioblast,

174 ere present in RapGEF2(+/+) and RapGEF2(-/-) yolk sacs indicating that the bipotential early progenit

175 We detected a capD transcript in yolk sacs infected with R. prowazekii at ten days post-i

176 nt of the primitive erythroid lineage in the yolk sac is a temporally and spatially restricted progra

177 y, vascular remodeling of the extraembryonic yolk sac is abnormal in Brg1(fl/fl):Tie2-Cre(+) embryos.

178 show that TRPM6 activity in the placenta and yolk sac is essential for embryonic development.

179 The yolk sac is phylogenetically the oldest of the extraembr

180 as shown that vessel remodeling in the mouse yolk sac is secondarily effected when cardiac function i

181 primitive endoderm (PE), which will form the yolk sac, is a crucial developmental decision.

182 ve erythropoiesis, beginning at E8.25 in the yolk sac, is completely c-myb-dependent.

183 oglossus): 2-cell stage (embryos), 1 day-old yolk sac larvae (trunk) and juvenile (fast skeletal musc

184 in European sea bass (Dicentrarchus labrax) yolk-sac larvae was explored.

185 obin switches are recapitulated, and because yolk sac-like and fetal liver-like cells are sequentiall

186 can generate endothelium and form organized, yolk sac-like structures that secondarily generate multi

187 e species indicates that the human secondary yolk sac likely performs key functions early in developm

188 e dorsal aorta, and only later appear in the yolk sac, liver, and placenta.

189 ty of organs in which substantial numbers of yolk-sac macrophages persisted in adulthood.

190 SIRT1(-/-) yolk sacs manifested fewer primitive erythroid precursor

191 In a chicken yolk sac membrane model, under the same ultrasound param

192 nic malformations, including ruffling of the yolk sac membrane, defective extraembryonic mesoderm mor

193 feration were confined to the YY1-expressing yolk sac mesoderm indicating that loss of YY1 in the vis

194 escued angiogenesis and apoptosis in the cKO yolk sac mesoderm, but also restored the epithelial defe

195 ponsive paracrine signal, originating in the yolk sac mesoderm, is required to promote normal viscera

196 eral endoderm causes defects in the adjacent yolk sac mesoderm.

197 responsible for this vascular defect was the yolk sac mesothelial cells, not the cardiomyocytes or th

198 nstrate that PDGF receptors cooperate in the yolk sac mesothelium to direct blood vessel maturation a

199 ibed roles of the extraembryonic mesoderm in yolk sac morphogenesis and in the closure of the ectopla

200 ating red blood cells and exhibited abnormal yolk sac morphology at 48 h post-fertilization.

201 ve yolk sac vasculogenesis, both cardiac and yolk sac morphology of Tmod1(-/-Tg(alphaMHC-Tmod1)) embr

202 Blood vessels were absent in the yolk sac of DGCR8 KOs after E12.5.

203 The vascular structure was absent in the yolk sac of Drosha homozygotes at E14.5.

204 and TC-(57)CoB12 accumulated in the visceral yolk sac of KO mice where megalin is expressed and provi

205 Hematopoiesis initiates within the yolk sac of mammalian embryos in overlapping primitive a

206 ein expression disappeared from the visceral yolk sac of RFC1-/- embryos, while cubilin protein was w

207 progenitors (EMPs) that first appear in the yolk sac of the early developing embryo.

208 (2)(1)(0)Po also accumulates in the yolk sac of the embryo and in the fetal and placental ti

209 (0)-resins can be carefully implanted in the yolk sac of zebrafish embryos and display excellent bioc

210 In yolk sacs of mutant embryos, endothelial cells formed a

211 on of the allantois that are unavailable for yolk sac or dorsal aorta, and review how this system has

212 hat FcRn is expressed in the endoderm of the yolk sac placenta but not in other cells of the yolk sac

213 placenta, we have studied FcRn in the mouse yolk sac placenta in detail.

214 k sac placenta but not in other cells of the yolk sac placenta or in the chorioallantoic placenta.

215 tic cues that drive the morphogenesis of the yolk sac placenta.

216 ls, termed hemogenic endothelium, within the yolk sac, placenta, and aorta.

217 ults in abnormal vascular development in the yolk sac, placenta, and brain.

218 y give rise to chorio-allantoic and visceral yolk sac placentae, respectively.

219 the endoderm of both FcRn(+/+) and FcRn(-/-) yolk sac placentas and in the mesenchyme of FcRn(+/+) bu

220 was missing from the mesenchyme of FcRn(-/-) yolk sac placentas, indicating that IgG enters the endod

221 Resident macrophages are derived from yolk sac precursors and seed the liver during embryogene

222 In contrast, microglia and their yolk sac precursors develop independently of IL-34 but r

223 od vessel formation as determined by lack of yolk sac primary capillary plexus formation and disorgan

224 nd with definitive erythroid lineages in the yolk sac prior to the transition of hematopoiesis to int

225 tiple progenitor pools, microglia arise from yolk sac progenitors and are widely considered to be equ

226 ng early embryogenesis, microglia arise from yolk sac progenitors that populate the developing centra

227 ies were observed in the T(C)/T(C) heart and yolk sac, recently reported sites of T localization.

228 ptor 2(+) macrophages derived from primitive yolk sac, recombination activating gene 1(+) lymphomyelo

229 with dilated pericardial sacs and failure of yolk sac remodeling suggestive of cardiovascular failure

230 e made earlier, that displayed labyrinth and yolk sac-specific defects, but our findings extend those

231 protein is a rodent-specific, placenta- and yolk sac-specific member of the tristetraprolin (TTP) fa

232 uced levels of VEGFA are observed in the cKO yolk sac, suggesting a cause for the angiogenesis defect

233 ells, identifying the earliest stages in the yolk sac, throughout embryonic development and in all ad

234 bryonic vascular development, was reduced in yolk sac tissues of zimp10 null embryos.

235 endoderm (PrE), which forms extra-embryonic yolk sac tissues.

236 al IgY in egg yolk is transferred across the yolk sac to passively immunize chicks during gestation a

237 d vascular abnormalities seen in Brg1 mutant yolk sacs to the same extent as LiCl treatment.

238 into embryonal carcinoma (EC), teratoma (T), yolk sac tumor (YS), and choriocarcinoma (CC) on the bas

239 monitoring for early detection of malignant yolk sac tumor (YST) recurrence, were recommended.

240 associated with worse outcome, whereas pure yolk sac tumor (YST) was associated with better outcome,

241 s differentiated derivatives, teratoma (TE), yolk sac tumor (YST), and choriocarcinoma.

242 malignant histologic types of pediatric GCT, yolk sac tumor (YST; n = 18), and seminoma (n = 9).

243 my, which revealed a 5-cm tumor that was 95% yolk sac tumor and 5% embryonal carcinoma, and retroperi

244 of Mexican-born mothers had a higher risk of yolk sac tumors (HR, 1.46; 95% CI, 0.99-2.17), while chi

245 ere identified in teratomas (EGR1 and MMP7), yolk sac tumors (PTPN13 and FN1), and seminomas (NR6A1,

246 d major dysplasia and malignant tumors, with yolk sac tumors and embryonal carcinomas positive for al

247 ial lipodystrophy and a history of childhood yolk sac tumour.

248 nign teratoma, epidermoid cyst and malignant yolk-sac tumours) and stromal tumours (such as juvenile

249 tic progenitor that gives rise to primitive (yolk sac-type) erythrocytes and megakaryocytes.

250 into the extra-embryonic region to form the yolk sac, umbilical cord and placenta.

251 Several of these mutants also display yolk sac vascular defects, suggesting a role for thrombi

252 embryonic lethality at ~ E11.5 due to severe yolk sac vascular defects.

253 Brg1 mutants, Chd4 mutant embryos had normal yolk sac vascular morphology.

254 Nonetheless, development of an organized yolk sac vascular plexus failed in Yap-/- embryos.

255 severe defects in the reorganization of the yolk sac vascular plexus.

256 Brg1 from embryonic blood vessels results in yolk sac vascular remodeling defects.

257 at PITX2 helps to mediate the restoration of yolk sac vascular remodeling under both conditions.

258 oid rescue experiments reveals that abnormal yolk-sac vascularization is the probable cause of lethal

259 than 90% of Mpi(-/-) embryos failed to form yolk sac vasculature, and 35% failed chorioallantoic fus

260 ts in angiogenic remodeling of embryonic and yolk sac vasculature, cardiac development, smooth muscle

261 orrhage, failure of remodeling embryonic and yolk sac vasculature, defective placental angiogenesis a

262 ial for normal growth and development of the yolk sac vasculature.

263 Wnt signaling was upregulated in Chd4 mutant yolk sac vasculature.

264 lethality may be attributable to defects in yolk sac vasculogenesis and angiogenesis.

265 diated activation of Tbeta4 is essential for yolk sac vasculogenesis and embryonic survival, and admi

266 wnstream target of Hand1 and reveal impaired yolk sac vasculogenesis as a primary cause of early embr

267 o undergo cardiac looping and have defective yolk sac vasculogenesis, both cardiac and yolk sac morph

268 nt for YAP in the developmental processes of yolk sac vasculogenesis, chorioallantoic attachment, and

269 primitive erythroid cells, and an absence of yolk sac vasculogenesis, followed by embryonic lethality

270 erythroid cells affect cardiac development, yolk sac vasculogenesis, or viability in the mouse.

271 oid cell fragility and subsequent defects in yolk sac vasculogenesis, we expressed Tmod1 specifically

272 terization revealed a requirement for YAP in yolk sac vasculogenesis.

273 For in utero gene delivery, we did yolk sac vessel injection at midgestation of mouse embry

274 N629D/N629D yolk sac vessels and aorta consist of sinusoids without

275 e the ability to roll and adhere on inflamed yolk sac vessels during late fetal development, whereas

276 Yolk sac vessels in the E10.5 null mutant fail to remode

277 g, adhesion, and extravasation from inflamed yolk sac vessels is apparent late in development, but th

278 tically modulate Wnt signaling in developing yolk sac vessels to mediate normal vascular remodeling.

279 is initially expressed only in the visceral yolk sac (VYS) endoderm and shows a highly restricted pa

280 ulturing isolated E11.5 AGM region and E12.5 yolk sac we show that the developmental switch from a ;p

281 As previously reported for INS in the yolk sac, we demonstrate complex, tissue-specific imprin

282 Capillaries and intercapillary spaces in yolk sacs were dilated before any other detectable abnor

283 Capillaries of the yolk sacs were disorganized, and the endothelium of majo

284 ressed predominantly in blood islands of the yolk sac, where endothelial and hematopoietic cells deve

285 The human embryo retains a yolk sac, which goes through primary and secondary phase

286 Subsequently, definitive MEPs expand in the yolk sac with Meg-CFCs and definitive erythroid progenit

287 While yolk sac (YS) also contained lymphopoietic cells after E

288 denocarcinoma (PDAC) originate from both the yolk sac (YS) and bone marrow.

289 ro MF-depletion strategy and fate-mapping of yolk sac (YS) and fetal liver (FL) hematopoiesis.

290 lack systemic blood circulation, that the E9 yolk sac (YS) and the intra-embryonic para-aortic splanc

291 During chicken yolk sac (YS) growth, mesodermal cells in the area vascu

292 The extra-embryonic yolk sac (YS) is the first hematopoietic site in the mou

293 tes and macrophages, but was dispensable for yolk sac (YS) macrophages and for the development of YS-

294 evidence that support either extra-embryonic yolk sac (YS) macrophages or hematopoietic stem cells (H

295 enitor/colony-forming cells of the embryonic yolk sac (YS), which are endowed with megakaryocytic pot

296 The relative contribution of yolk sac (YS)-derived cells to the circulating definitiv

297 lineage tracing, we identify a first wave of yolk sac (YS)-derived primitive myeloid progenitors that

298 t ACE+CD45-CD34+/- hemangioblasts are common yolk sac (YS)-like progenitors for not only endothelium

299 cluding impaired vascular development in the yolk sac (YS).

300 lose association in the blood islands of the yolk sac (YS).