ライフサイエンスコーパス: cytotrophoblast

1 acental villi was predominantly localized to cytotrophoblast.

2 vels of growth factor signaling mediators in cytotrophoblast.

3 to 252-fold compared with directly infected cytotrophoblasts.

4 questions about its physiological impact on cytotrophoblasts.

5 dothelial cells and differentiating-invading cytotrophoblasts.

6 dent expression of syncytin 1 and 2 in human cytotrophoblasts.

7 ized predominantly to the cytoplasm of human cytotrophoblasts.

8 ace to changes in the biological behavior of cytotrophoblasts.

9 iptionally attenuated at term as observed in cytotrophoblasts.

10 maintain Id-2 protein expression in cultured cytotrophoblasts.

11 structural changes without interaction with cytotrophoblasts.

12 gulators controlling self-renewal of villous cytotrophoblasts.

13 trophoblast and the villous and extravillous cytotrophoblasts.

14 ncytin 2, but not hCG beta, in primary human cytotrophoblasts.

15 ression in vascular endothelial cells and in cytotrophoblasts.

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

17 These cytotrophoblasts aggregate into cell columns and invade

18 Cytotrophoblasts also produce human interleukin-10 (hIL-

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

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

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

22 te the expression of CSF-1R and CSF-1 in the cytotrophoblast and syncytiotrophoblast within ectopic i

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

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

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

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

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

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

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

30 immunoreactivity in extravillous (invasive) cytotrophoblasts and syncytial sprouts vs. villous troph

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

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

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

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

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

36 first time that the syncytiotrophoblast and cytotrophoblast are a major site of STC-1 protein expres

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

38 Villous cytotrophoblasts are epithelial stem cells of the early

39 Cytotrophoblasts are specialized epithelial cells of the

40 chanisms that govern appropriate invasion of cytotrophoblasts are unknown.

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

42 As cytotrophoblasts attached to and invaded the uterus, whi

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

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

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

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

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

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

49 re impeded the interaction between the human cytotrophoblast cell line, HTR-8/SVneo, and endothelium

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

51 F-2 primarily to decidual cell cytoplasm and cytotrophoblast cell membranes.

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

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

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

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

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

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

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

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

60 Invasive cytotrophoblast cells differentiate from precursor villo

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

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

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

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

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

66 Treatment of primary human cytotrophoblast cells with NPFF increased the mRNA and p

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

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 CM1)] genes in first trimester primary human cytotrophoblast cells.

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

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

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

75 yncytiotrophoblast and invasive extravillous cytotrophoblast cells.

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

77 Cytotrophoblasts colonizing spiral arterioles replace ma

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

79 Additionally, cytotrophoblast commitment to uterine invasion was accom

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

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

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

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

84 s a key regulator for the differentiation of cytotrophoblast (CT) into syncytiotrophoblast (ST).

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

86 Cytotrophoblast (CTB) aggregates that bridge the gap bet

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

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

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

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

91 During human placentation, villous cytotrophoblast (CTB) progenitors differentiate to form

92 tein 1 (YAP1), are specifically expressed in cytotrophoblast (CTB) progenitors of a first-trimester h

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

94 We isolated EVs from second trimester human cytotrophoblasts (CTBs) by differential ultracentrifugat

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

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

97 Extravillous cytotrophoblasts (CTBs) fail to differentiate properly,

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

99 In humans, a subset of placental cytotrophoblasts (CTBs) invades the uterus and its vascu

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

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

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

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

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

105 ells augment ZIKV infection of primary human cytotrophoblast cultures, which are otherwise ZIKV resis

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

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

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

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

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

111 ease from proximal to distal cell columns as cytotrophoblasts differentiate into invasive EVTs.

112 Placental cytotrophoblasts differentiate, assume an endothelial ph

113 As cytotrophoblasts differentiate, they acquire tumor-like

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

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

116 Cytotrophoblast differentiation and invasion during the

117 CMV infection impairs cytotrophoblast differentiation and invasion, altering t

118 pha and HIF2alpha expression patterns during cytotrophoblast differentiation into syncytiotrophoblast

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

120 When cytotrophoblast differentiation was compromised (hypoxia

121 In cases when cytotrophoblast differentiation was compromised (in plac

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

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

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

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

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

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

128 When cytotrophoblasts encounter EPHB4 expressed by venous end

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

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

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

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

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 first and second trimester placental villous cytotrophoblasts followed by culture in TSC medium to ma

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

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

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

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

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

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

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

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

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

163 Cytotrophoblasts in cell columns show reduced E-cadherin

164 ross syncytiotrophoblasts, infect underlying cytotrophoblasts in chorionic villi.

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

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

167 rivation, but give rise to non-self-renewing cytotrophoblasts in response to BMP4.

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

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

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

171 ranes, and 2) non-proliferative interstitial cytotrophoblasts in the placental villi.

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

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

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

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

176 Cytotrophoblast incubated for the longest time period st

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

178 nfected decidual cell supernatants increased cytotrophoblasts infection up to 252-fold compared with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Cytotrophoblast invasion in vitro requires the expressio

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

195 Cytotrophoblast invasion of the kidney parenchyma was ac

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

197 Cytotrophoblast invasion under these conditions is also

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

199 ceptus attaches itself to the uterus through cytotrophoblast invasion.

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

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

202 increased when syncytialization of cultured cytotrophoblasts is progressed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Invasive extravillous cytotrophoblast of the human placenta expresses galectin

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

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

221 Cytotrophoblasts of the anchoring villi convert during h

222 Mononuclear cytotrophoblasts of the human placenta proliferate rapid

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

224 Genome-wide comparisons of primary villous cytotrophoblasts overexpressing constitutively active YA

225 CSF2 mRNA was higher in TDCs versus cytotrophoblasts (P < 0.05), whereas CSF2R mRNA was 1.3

226 The data show that cytotrophoblasts predominantly expressed Ang2.

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

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

229 o signaling pathway, promotes maintenance of cytotrophoblast progenitors by different genomic mechani

230 asive extravillous trophoblasts derived from cytotrophoblast progenitors remodel maternal arterioles

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

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

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

234 Paradoxically, human cytotrophoblasts proliferate under hypoxic conditions co

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

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

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

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

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

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

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

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

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

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

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

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

247 ndividual chemokine receptors suggested that cytotrophoblasts secreted monocyte inflammatory protein

248 Cytotrophoblast secretion of the soluble form of VEGFR-1

249 -2 was expressed by CTB in cell columns, the cytotrophoblast shell, and cell islands.

250 Differentiated primary villous cytotrophoblasts showed that CORIN was expressed (mRNA a

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

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

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

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

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

259 enes critical for maintaining the epithelial cytotrophoblasts stem cell phenotype.

260 oxia or differentiation of iPSCs into either cytotrophoblast-stem-like cells or EVT-like cells under

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

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

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

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

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

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

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

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

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

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

271 Within cytotrophoblast, the rough endoplasmic reticulum incorpo

272 Cytotrophoblasts, their conditioned medium, and amniotic

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

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

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

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

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

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

279 During implantation, cytotrophoblasts undergo epithelial-to-mesenchymal trans

280 During invasion, ectodermally derived cytotrophoblasts undergo pseudovasculogenesis, switching

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

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

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

284 sembles the villous placenta with a layer of cytotrophoblast (VCT) that differentiates into superimpo

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

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

287 as CSF2R mRNA was 1.3 x 10(4)-fold higher in cytotrophoblasts versus TDCs (P < 0.001).

288 Cytotrophoblast, villous stroma, and Hofbauer cells show

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

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

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

292 Isolated cytotrophoblasts were also permissive for CMV replicatio

293 Primary cultures of placental cytotrophoblasts were differentiated into syncytiotropho

294 Villous cytotrophoblasts were isolated from 7 placentas of obese

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.