ライフサイエンスコーパス: cytotrophoblast

1 vels of growth factor signaling mediators in cytotrophoblast.

2 acental villi was predominantly localized to cytotrophoblast.

3 questions about its physiological impact on cytotrophoblasts.

4 dothelial cells and differentiating-invading cytotrophoblasts.

5 ized predominantly to the cytoplasm of human cytotrophoblasts.

6 gulators controlling self-renewal of villous cytotrophoblasts.

7 ace to changes in the biological behavior of cytotrophoblasts.

8 iptionally attenuated at term as observed in cytotrophoblasts.

9 maintain Id-2 protein expression in cultured cytotrophoblasts.

10 structural changes without interaction with cytotrophoblasts.

11 a molecule expressed preferentially on fetal cytotrophoblasts.

12 trophoblast and the villous and extravillous cytotrophoblasts.

13 ression in vascular endothelial cells and in cytotrophoblasts.

14 icantly, infection subsequently impaired the cytotrophoblasts' ability to differentiate and invade.

15 These cytotrophoblasts aggregate into cell columns and invade

16 Cytotrophoblasts also produce human interleukin-10 (hIL-

17 c-MYC proteins coexpressed in proliferating cytotrophoblast and coordinately lost in postmitotic syn

18 at FASN immunoreactivity was detected in the cytotrophoblast and intermediate (extravillous) trophobl

19 lity of human placental trophoblast to ZIKV: cytotrophoblast and syncytiotrophoblast derived from pla

20 with subsequent infection of the underlying cytotrophoblasts and (ii) via invasive cytotrophoblasts

21 f primary trophoblasts as well as of villous cytotrophoblasts and cell column trophoblasts in placent

22 and/or cell-matrix interactions of infected cytotrophoblasts and endothelial cells.

23 NA and protein expression in human placental cytotrophoblasts and explant cultures in a dose- and tim

24 ute homologue 2), which is elevated in human cytotrophoblasts and maintained at elevated levels by hy

25 cytiotrophoblasts were often spared, whereas cytotrophoblasts and other cells of the villous core exp

26 VR1814 replicated in villous and cell column cytotrophoblasts and reduced formation of anchoring vill

27 coprotein synthesis in cellular trophoblast (cytotrophoblast) and syncytial trophoblast of term human

28 on molecule highly expressed by endovascular cytotrophoblasts, and increased apoptosis.

29 villi of the rhesus placenta, within villous cytotrophoblasts, and occasionally within cells of the v

30 um and lymphatic endothelium in the decidua, cytotrophoblasts, and smooth muscle cells in blood vesse

31 rmal differentiation and/or hypoxia leads to cytotrophoblast apoptosis, we used the TUNEL (terminal d

32 On the other hand, when cytotrophoblasts are cultured in 2% O(2), syncytiotropho

33 Villous cytotrophoblasts are epithelial stem cells of the early

34 Cytotrophoblasts are specialized epithelial cells of the

35 chanisms that govern appropriate invasion of cytotrophoblasts are unknown.

36 r eNOS or iNOS was expressed by extravillous cytotrophoblasts at any time during invasion.

37 As cytotrophoblasts attached to and invaded the uterus, whi

38 In vitro cytotrophoblasts avoided EPHB4-coated substrates; upon c

39 t cells differentiate from precursor villous cytotrophoblasts, but the essential regulating factors i

40 d that this process was initiated in primary cytotrophoblasts by histone H3K4 di- and trimethylation

41 se data suggest the specific conclusion that cytotrophoblasts can attract monocytes and CD56(bright)

42 Here we tested the hypothesis that fetal cytotrophoblasts can direct the migration of these mater

43 ovascular and intravascular cytotrophoblast, cytotrophoblast cell columns, and syncytiotrophoblast of

44 lel in a cell model of syncytialization (the cytotrophoblast cell line BeWo following increased intra

45 g a well-characterized human first trimester cytotrophoblast cell line, we found that a 4-hour exposu

46 lls (-25 mV) than in mono- and multinucleate cytotrophoblast cells (-33 and -43 mV, respectively).

47 al metabolism, and the underlying progenitor cytotrophoblast cells (CTB) an insignificant contributor

48 ressed within the placenta and that invading cytotrophoblast cells (CTB) express HO isoforms.

49 female and three male concepti), and villous cytotrophoblast cells (vCTBs) were isolated at 15-20 wk

50 Although both isolated placental villous cytotrophoblast cells and chorion membrane extravillous

51 and TR6 (DcR3)] are present in placentas and cytotrophoblast cells at term.

52 ncrease (4.5%) in cell water in mononucleate cytotrophoblast cells but lowered K+ (approximately 30%)

53 was similar in JAr, mono- and multinucleate cytotrophoblast cells but Na+ concentration was higher i

54 s expressed in the human placenta in villous cytotrophoblast cells but not in post-mitotic syncytiotr

55 Na+ concentration was higher in mononucleate cytotrophoblast cells compared with JAr cells.

56 last cells and chorion membrane extravillous cytotrophoblast cells contained mRNAs encoding sG1 and s

57 ve ELF5(+)/CDX2(+) double-positive subset of cytotrophoblast cells demarcates a putative TS cell comp

58 Invasive cytotrophoblast cells differentiate from precursor villo

59 his paradigm exists in human placenta, where cytotrophoblast cells either propagate or undergo a uniq

60 was required to suppress genes that maintain cytotrophoblast cells in a progenitor state, including M

61 chemistry, TRPC3 and TRPC4 were localised to cytotrophoblast cells in first trimester placentas and t

62 onucleate and multinucleate (differentiated) cytotrophoblast cells isolated from the human placenta a

63 n were expressed in villous and extravillous cytotrophoblast cells up to week 35 of gestation in plac

64 centas, amniochorion membranes, and purified cytotrophoblast cells were evaluated by immunoblotting a

65 rly and late gestation human placentas, term cytotrophoblast cells, and two choriocarcinoma cell line

66 ma-derived cell line (JAr) which, unlike the cytotrophoblast cells, divides in culture, was also stud

67 to -48 and -40 mV in mono-and multinucleate cytotrophoblast cells, respectively.

68 oinflammatory profile in isolated human term cytotrophoblast cells, with a predominant secretion of I

69 es, is expressed by leukocytes and chorionic cytotrophoblast cells.

70 tein was present exclusively in extravillous cytotrophoblast cells.

71 s and all receptors were in low abundance in cytotrophoblast cells.

72 localized the signal to the layer of villous cytotrophoblast cells.

73 ent, we first characterized Id expression in cytotrophoblast cells.

74 significantly lower in 66 vs. 18 h cultured cytotrophoblast cells.

75 Na(+)-K(+)-ATPase during differentiation of cytotrophoblast cells.

76 or Na+ is similar in mono- and multinucleate cytotrophoblast cells.

77 yncytiotrophoblast and invasive extravillous cytotrophoblast cells.

78 ed in decidual areas containing interstitial cytotrophoblasts clearly less amount of TUNEL-positive c

79 Cytotrophoblasts colonizing spiral arterioles replace ma

80 pecialized epithelial cells of the placenta (cytotrophoblasts) come into direct contact with immune c

81 Additionally, cytotrophoblast commitment to uterine invasion was accom

82 roto-oncogene was increased in proliferating cytotrophoblasts compared to that in differentiated sync

83 irst, we assayed the chemotactic activity of cytotrophoblast conditioned medium samples, using human

84 Immunodepletion of MIP-1alpha from cytotrophoblast conditioned medium showed that this chem

85 g uterine microvascular endothelial cells in cytotrophoblast-conditioned medium, which supported thei

86 Terminal differentiation of villous cytotrophoblasts (CT) ends in formation of the multinucl

87 Cytotrophoblast (CTB) aggregates that bridge the gap bet

88 emonstrated that MBG impairs first trimester cytotrophoblast (CTB) cell proliferation, migration, and

89 Here, we investigated mechanisms protecting cytotrophoblast (CTB) cells from LIGHT-mediated apoptosi

90 Although proximally continuous with villous cytotrophoblast (CTB) distally, these cells differentiat

91 In preeclampsia (PE), cytotrophoblast (CTB) invasion of the uterus and spiral

92 lear proteins, is expressed in proliferative cytotrophoblast (CTB), precursors to terminally differen

93 Primary first-trimester cytotrophoblasts (CTBs) derived from the placenta exhibi

94 uring human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that a

95 Extravillous cytotrophoblasts (CTBs) fail to differentiate properly,

96 r TLR3 activation in pregnant mice and human cytotrophoblasts (CTBs) increases miR-210 and modulates

97 Primary cytotrophoblasts (CTBs) isolated from early-gestation (6

98 Studies of primary cytotrophoblasts (CTBs) revealed that HCMV infection imp

99 Cultured cytotrophoblasts (CTs) and an in vitro model of syncytia

100 In this study, cytotrophoblasts cultured under hypoxic conditions (2 pe

101 Adding recombinant IL-10 to cytotrophoblast cultures significantly decreased the cel

102 tero and that LIMK1 activity regulated human cytotrophoblast cytoskeletal integrity, matrix metallope

103 otrophoblast, endovascular and intravascular cytotrophoblast, cytotrophoblast cell columns, and syncy

104 could mediate cytotrophoblast-endothelium or cytotrophoblast-cytotrophoblast interactions in vivo, du

105 miRNA microarray analysis of RNA from human cytotrophoblasts (CytT), before and after differentiatio

106 We also assayed the angiogenic potential of cytotrophoblast-derived factors in the chick chorioallan

107 at it partners play important roles in human cytotrophoblast development.

108 Placental cytotrophoblasts differentiate, assume an endothelial ph

109 As cytotrophoblasts differentiate, they acquire tumor-like

110 hoblasts) and anchoring villi (which include cytotrophoblasts differentiating into invasive cells).

111 that contained floating villi (which include cytotrophoblasts differentiating into syncytiotrophoblas

112 Cytotrophoblast differentiation and invasion during the

113 CMV infection impairs cytotrophoblast differentiation and invasion, altering t

114 ated whether lowering oxygen tension affects cytotrophoblast differentiation and invasion.

115 pha and HIF2alpha expression patterns during cytotrophoblast differentiation into syncytiotrophoblast

116 y HB-EGF or other EGF family members induces cytotrophoblast differentiation to an invasive phenotype

117 When cytotrophoblast differentiation was compromised (hypoxia

118 In cases when cytotrophoblast differentiation was compromised (in plac

119 Preeclampsia is associated with abnormal cytotrophoblast differentiation, shallow invasion, and d

120 ons for these molecules, including a role in cytotrophoblast differentiation.

121 These results suggest that defective cytotrophoblast differentiation/invasion can have signif

122 ese changes mimic many of the alterations in cytotrophoblast differentiation/invasion that occur in p

123 f the miR-17~92 and miR-106a~363 clusters in cytotrophoblasts dramatically decreased upon syncytiotro

124 st majority of the [3H]gal incorporated into cytotrophoblast during the pulse incubation remained int

125 the invasive and cell surface properties of cytotrophoblasts enable them to form vascular connection

126 When cytotrophoblasts encounter EPHB4 expressed by venous end

127 placental attachment to the mother, invasive cytotrophoblasts encounter specialized maternal natural

128 s primary human placental cells and explants-cytotrophoblasts, endothelial cells, fibroblasts, and Ho

129 esting that this receptor-pair could mediate cytotrophoblast-endothelium or cytotrophoblast-cytotroph

130 unknown, but are likely to affect negatively cytotrophoblast endovascular invasion and uterine arteri

131 a parallel process is important for enabling cytotrophoblast endovascular invasion during human pregn

132 d immunoreactive EPO associated with villous cytotrophoblast, endovascular and intravascular cytotrop

133 By an unknown mechanism, invasive cytotrophoblasts exhibit permanent cell cycle withdrawal

134 ve for all proteins whereas chorion membrane cytotrophoblasts exhibited none.

135 is study tested the hypothesis that invading cytotrophoblasts express NOS and therefore have the pote

136 Previously, we have shown that invasive cytotrophoblasts express several chemokines, as well as

137 Infected cytotrophoblasts expressed CMV IL-10 (cmvIL-10) mRNA and

138 gical study in the guinea pig suggested that cytotrophoblasts expressed nitric oxide synthase (NOS) a

139 me infected, although clusters of underlying cytotrophoblasts expressed viral proteins.

140 Cytotrophoblasts expressing alpha4 integrins bound immob

141 In the decidua, invasive cytotrophoblasts expressing coreceptors upregulate EGFR,

142 dings indicate that virion interactions with cytotrophoblasts expressing receptors in the placenta (i

143 n, we used an adenovirus strategy to inhibit cytotrophoblast expression of FAK as the cells different

144 in which endovascular invasion is abrogated, cytotrophoblasts fail to adopt a vascular adhesion pheno

145 h endovascular invasion remains superficial, cytotrophoblasts fail to express most of these endotheli

146 It was also reported that in preeclampsia, cytotrophoblasts fail to express PECAM-1 and that failur

147 In preeclampsia, differentiating/invading cytotrophoblasts fail to express properly many of these

148 ental tissue, that in pre-eclampsia invasive cytotrophoblasts fail to properly modulate their integri

149 Cytotrophoblasts from all stages of pregnancy produced I

150 14 isolated villous cytotrophoblasts from control (n = 3), IUGR (n = 3), PE

151 or in placental explants or freshly isolated cytotrophoblasts from different gestational ages and com

152 at CMV infection impairs critical aspects of cytotrophoblast function offers testable hypotheses for

153 This insufficiency involves impaired cytotrophoblast functions, including reduced migration a

154 gonadotropin (CG), increases dramatically as cytotrophoblasts fuse to form syncytiotrophoblasts.

155 When cultured in 20% O(2), human cytotrophoblasts fuse to form the syncytiotrophoblast wi

156 When cultured in 2% O(2), cytotrophoblast fusion and induced hCYP19 expression are

157 Disruption of OVOL1 abrogated cytotrophoblast fusion and inhibited the expression of a

158 indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be importan

159 horiocarcinoma cell line, a model of villous cytotrophoblast fusion.

160 tion process, human trophoblast progenitors (cytotrophoblasts) give rise to tumor-like cells that inv

161 In xenografts, infected cytotrophoblasts had a severely diminished capacity to i

162 , and decidual areas containing interstitial cytotrophoblasts have numerous TUNEL-positive cells.

163 We conclude that human cytotrophoblast IL-10 may be an important factor that co

164 sue sections showed that FAK is expressed by cytotrophoblasts in all stages of differentiation.

165 Cytotrophoblasts in cell columns show reduced E-cadherin

166 ross syncytiotrophoblasts, infect underlying cytotrophoblasts in chorionic villi.

167 Invasive cytotrophoblasts in early gestation expressed VEGF-A, VE

168 In contrast, AD169 grew poorly in cytotrophoblasts in explants, and anchoring villi formed

169 experiments showed that both amniocytes and cytotrophoblasts in the amnion-chorion express this prot

170 Virus replicates in invasive cytotrophoblasts in the decidua, and maternal immunoglob

171 r (P < 0.01), and the receptors localized to cytotrophoblasts in the first trimester and to syncytiot

172 Cytotrophoblasts in the uterine interstitium and materna

173 tions nor 2-ME alone induces the invasion of cytotrophoblasts in this system; however, low-oxygen con

174 ting to study the HLA-G isoforms produced by cytotrophoblasts in vitro and by the amnion-chorion in v

175 IL-10 secreted by cytotrophoblasts in vitro is bioactive, as determined by

176 udied the vascular effects of invasive human cytotrophoblasts in vivo by transplanting placental vill

177 re placental cells, syncytiotrophoblasts and cytotrophoblasts, in chorionic villi-in clinical cases o

178 Cytotrophoblast incubated for the longest time period st

179 tors could undermine vascular remodeling and cytotrophoblast-induced lymphangiogenesis, contributing

180 As to the mechanisms involved, cytotrophoblast interactions with EPHB4 downregulated ch

181 ethyltransferase (COMT), induces invasion of cytotrophoblasts into a naturally-derived, extracellular

182 epidermal growth factor receptor(+) villous cytotrophoblasts into human leukocyte antigen-G(+) proxi

183 h 2-ME result in the appropriate invasion of cytotrophoblasts into the extracellular matrix.

184 At the uterine-placental interface, fetal cytotrophoblasts invade the decidua, breach maternal blo

185 this in vivo human placentation model, human cytotrophoblasts invade the renal parenchyma, remodel re

186 o endovascular invasion, the process whereby cytotrophoblasts invade the uterine spiral arterioles an

187 During early human pregnancy extravillous cytotrophoblasts invade the uterus and also migrate up t

188 During early human pregnancy extravillous cytotrophoblasts invade the uterus and spiral arteries t

189 ized placental cells of fetal origin, termed cytotrophoblasts, invade the uterus and its blood vessel

190 organ's specialized epithelial cells, termed cytotrophoblasts, invade the uterus where they reside in

191 -AG molecules are expressed predominantly in cytotrophoblasts invading the maternal vessels and endom

192 pregnancy associated with poor extravillous cytotrophoblast invasion and above-normal rates of apopt

193 rin receptors, is precisely modulated during cytotrophoblast invasion in situ.

194 Cytotrophoblast invasion in vitro requires the expressio

195 tion in endothelial cell wounding assays and cytotrophoblast invasion of Matrigel in vitro.

196 Cytotrophoblast invasion of the kidney parenchyma was ac

197 tions generate repulsive signals that direct cytotrophoblast invasion toward the uterus, where chemok

198 Cytotrophoblast invasion under these conditions is also

199 Over 3 weeks, robust cytotrophoblast invasion was observed in both locations.

200 ceptus attaches itself to the uterus through cytotrophoblast invasion.

201 ase pre-eclampsia is associated with shallow cytotrophoblast invasion.

202 t decrease in MMP activity, thereby reducing cytotrophoblast invasiveness.

203 adherin enhance, while E-cadherin restrains, cytotrophoblast invasiveness.

204 increased when syncytialization of cultured cytotrophoblasts is progressed.

205 Inadequate invasion of the uterus by cytotrophoblasts is speculated to result in pregnancy-in

206 acental tissues of various gestational ages, cytotrophoblasts isolated from term placenta, and JAR ch

207 (trophoblast-derived) choriocarcinoma cells, cytotrophoblasts isolated from term placenta, villous co

208 ed Hofbauer cells, and to a lesser extent in cytotrophoblasts, isolated from villous tissue of full-t

209 In cell columns, proximal cytotrophoblasts lack receptors and distal cells express

210 normal tissues is restricted to the invasive cytotrophoblast layer of the placenta; small interfering

211 In humans, fetal cytotrophoblasts leave the placenta and enter the uterin

212 Using a first-trimester human cytotrophoblast line, the potential for autocrine and pa

213 llowed the identification of 43 spots on the cytotrophoblast map.

214 oward the uterus, where chemokines stimulate cytotrophoblast migration through the decidua.

215 these ligand-receptor interactions stimulate cytotrophoblast migration to approximately the same leve

216 onent of the signaling pathway that mediates cytotrophoblast migration/invasion.

217 gest that IL-10 is an autocrine inhibitor of cytotrophoblast MMP-9 activity and invasiveness.

218 e whether IL-10 is an autocrine regulator of cytotrophoblast MMP-9 production.

219 experiments detected Y397FAK in a subset of cytotrophoblasts near the surface of the uterine wall.

220 he differentiative and invasive potential of cytotrophoblasts obtained from control (n = 8, 22 to 38

221 maternal leukocytes that co-exist with fetal cytotrophoblasts occupying the decidua and uterine blood

222 well as syncytiotrophoblast and extravillous cytotrophoblast of normal third-trimester and preeclampt

223 ibitory ligand expressed on the extravillous cytotrophoblast of the human placenta.

224 pecies, were increased in a subpopulation of cytotrophoblasts of preeclamptic women.

225 Cytotrophoblasts of the anchoring villi convert during h

226 Mononuclear cytotrophoblasts of the human placenta proliferate rapid

227 explants and differentiating and/or invading cytotrophoblasts offers an in vitro model for studying v

228 The data show that cytotrophoblasts predominantly expressed Ang2.

229 n early gestation, differentiating- invading cytotrophoblasts produce high levels of matrix metallopr

230 Recently, we showed that cytotrophoblasts produce interleukin-10 (IL-10), a poten

231 asive extravillous trophoblasts derived from cytotrophoblast progenitors remodel maternal arterioles

232 ing hypoxia, endothelial cells and placental cytotrophoblasts proliferate in response to low O(2).

233 Human cytotrophoblasts proliferate in vitro under low O(2) con

234 Thus, oxygen tension determines whether cytotrophoblasts proliferate or invade, thereby regulati

235 Paradoxically, human cytotrophoblasts proliferate under hypoxic conditions co

236 acental explants significantly reduced basal cytotrophoblast proliferation and expression of ERK and

237 ession differs between first trimester, when cytotrophoblast proliferation is rapid, and term, by whi

238 er new information about the early gestation cytotrophoblast protein repertoire and the generalized m

239 In vitro, hypoxia (2% O(2)) upregulated cytotrophoblast pVHL expression together with HIF2 alpha

240 The net effect is preferential cytotrophoblast remodeling of arterioles, a hallmark of

241 early in placental development could impair cytotrophoblast remodeling of the uterine vasculature an

242 It is therefore important to understand how cytotrophoblasts respond to changes in oxygen tension.

243 We also found that cytotrophoblasts responded to the VEGF ligands they prod

244 idization identified placental syncytial and cytotrophoblasts responsible for the synthesis of LOXL2

245 LX5, TLX1 and HOXA10 in primary term villous cytotrophoblast resulted in decreased proliferation and

246 replication was impaired in xenografts, and cytotrophoblasts retained invasive capacity, but some pa

247 Previously, we showed that invading cytotrophoblasts secrete VEGF-C and PlGF, factors that r

248 ndividual chemokine receptors suggested that cytotrophoblasts secreted monocyte inflammatory protein

249 Cytotrophoblast secretion of the soluble form of VEGFR-1

250 -2 was expressed by CTB in cell columns, the cytotrophoblast shell, and cell islands.

251 Scoring 12 chromosomes in flow-sorted cytotrophoblasts showed that more than 95% of the cells

252 pregnancy depends on the differentiation of cytotrophoblasts, specialized placental cells that physi

253 Cytotrophoblasts, specialized placental cells, prolifera

254 eviously we showed that when early gestation cytotrophoblast stem cells are cultured under standard c

255 During human placental development, cytotrophoblast stem cells differentiate and invade the

256 mal human pregnancy a subpopulation of fetal cytotrophoblast stem cells differentiate and invade the

257 During human placentation, fetal cytotrophoblast stem cells differentiate and then invade

258 rmal pregnancy, a subpopulation of placental cytotrophoblast stem cells executes an unusual different

259 nt of the human placenta requires that fetal cytotrophoblast stem cells in anchoring chorionic villi

260 In the fetal compartment of the placenta, cytotrophoblast stem cells lie adjacent to macrophages (

261 In situ, pVHL immunolocalized to villous cytotrophoblast stem cells, and expression was enhanced

262 portion of the uterus that contains invasive cytotrophoblasts, suggesting that this cytokine is also

263 udy showed that VEGF family members regulate cytotrophoblast survival and that expression of a subset

264 Virus replicates in the decidua, invasive cytotrophoblasts that breach the uterine vasculature and

265 rol cells transduced with a wild-type virus, cytotrophoblasts that expressed antisense FAK exhibited

266 Recent studies have suggested that cytotrophoblasts that invade spiral arteries mimic the e

267 In human pregnancy, placental cytotrophoblasts that invade the uterus downregulate the

268 a is associated with widespread apoptosis of cytotrophoblasts that invade the uterus.

269 otrophoblasts that cover chorionic villi and cytotrophoblasts that invade uterine vessels, suggesting

270 om patients with preeclampsia, 15-50% of the cytotrophoblasts that invaded the uterine wall were labe

271 n transcytosed virions reach EGFR-expressing cytotrophoblasts that selectively initiate expression of

272 protein repertoire of first trimester human cytotrophoblasts that were maintained under standard tis

273 Within cytotrophoblast, the rough endoplasmic reticulum incorpo

274 Mononuclear cytotrophoblasts, the specialized fetal cells of the pla

275 Cytotrophoblasts, their conditioned medium, and amniotic

276 lecule selectively expressed on extravillous cytotrophoblast; this cell type does not express convent

277 first-trimester chorionic villi and isolated cytotrophoblasts to CMV in vitro.

278 r along with 2-ME for the proper invasion of cytotrophoblasts to facilitate appropriate vascular deve

279 t preeclampsia is associated with failure of cytotrophoblasts to mimic a vascular adhesion phenotype.

280 This transformation allows cytotrophoblasts to replace the maternal cells that line

281 Compared to control (lacZ-expressing) cells, cytotrophoblasts transduced to constitutively express Id

282 We show here that differentiating cytotrophoblasts transform their adhesion receptor pheno

283 During invasion, ectodermally derived cytotrophoblasts undergo pseudovasculogenesis, switching

284 t breach the uterine vasculature and villous cytotrophoblasts underlying syncytiotrophoblasts, then r

285 Results show that embryonic cytotrophoblasts up-regulated Mig-7 expression before th

286 These data suggest that invasive human cytotrophoblasts use an unusual repertoire of factors to

287 e subpopulations of placental cells, villous cytotrophoblast (vCTB) cells and mesenchymal cells (MCs)

288 olocalization on tissue sections showed that cytotrophoblast VEGF-A and VEGFR-1 staining decreased; s

289 Cytotrophoblast, villous stroma, and Hofbauer cells show

290 The expression of NOS on extravillous cytotrophoblasts was studied in placental bed biopsies,

291 Using primary cytotrophoblasts, we determined that culture in low oxyg

292 d with decidual areas devoid of interstitial cytotrophoblasts, we observed in decidual areas containi

293 Isolated cytotrophoblasts were also permissive for CMV replicatio

294 Primary cultures of placental cytotrophoblasts were differentiated into syncytiotropho

295 MV replication proteins in underlying villus cytotrophoblasts, whereas syncytiotrophoblasts were spar

296 When human cytotrophoblasts, which lack the capacity to express aro

297 Fusion of placental villous cytotrophoblasts with the overlying syncytiotrophoblast

298 ith 4H84 confirmed our previous finding that cytotrophoblasts within the uterine wall are the only ce

299 lying cytotrophoblasts and (ii) via invasive cytotrophoblasts within the uterine wall.

300 the proliferative and invasive potential of cytotrophoblasts within the uterus.