ライフサイエンスコーパス: trophoblast

1 s on the defining cell of the placenta - the trophoblast.

2 teria monocytogenes (Lm) without killing the trophoblast.

3 , and increased invasion of the extravillous trophoblast.

4 n of imprinting gene expression in the molar trophoblast.

5 DLX5 is expressed in human but not in murine trophoblast.

6 ophoblasts and syncytial sprouts vs. villous trophoblasts.

7 at IFN blocks fusion of BeWo human placental trophoblasts.

8 tress and antiangiogenic response in hypoxic trophoblasts.

9 ne kinase 1 (sFLT1), and soluble endoglin in trophoblasts.

10 ided with an increased frequency of infected trophoblasts.

11 ly target InsRs in fetally derived placental trophoblasts.

12 ar results were obtained with HUVEC and HTR8 trophoblasts.

13 in human term decidual stromal cells versus trophoblasts.

14 es in the differentiation of human placental trophoblasts.

15 uronidase was also stimulated in NS1-treated trophoblasts.

16 ha differentially affects gene expression in trophoblast and embryonic stem cells.

17 tures (ETX-embryoids) using mouse embryonic, trophoblast and extra-embryonic endoderm stem cells.

18 te antigens HLA-G and HLA-F are expressed on trophoblast and malignant cells.

19 and stimulates oxidative phosphorylation in trophoblast and that ETC protein expression is down-regu

20 entas displayed strong expression in villous trophoblasts and a gradual decrease from proximal to dis

21 tion via modulation of glycosaminoglycans on trophoblasts and chorionic villi, resulting in increased

22 4 causes ferroptotic injury in primary human trophoblasts and during mouse pregnancy.

23 fection induced autophagic activity in human trophoblasts and pharmacological inhibition limited ZIKV

24 We measured changes in permeability in trophoblasts and stromal cores using a dextran-based flu

25 We show that ACKR2 is strongly expressed by trophoblasts and that it blocks movement of inflammatory

26 in the functional regulation of extravillous trophoblasts and the development of PE remains unknown.

27 y tube formation involving HUVEC and/or HTR8 trophoblasts, and aortic ring endothelial cell outgrowth

28 and BeWo cells and in primary human villous trophoblasts, and this induction was abrogated by CH2231

29 ry effect of MSU crystals was accompanied by trophoblast apoptosis and decreased syncytialization.

30 ed effects on inflammatory cytokine release, trophoblast apoptosis and proliferation compared to cont

31 vere preeclampsia, PZP-positive extravillous trophoblasts are adjacent to extracellular plaques conta

32 However, these small quantities of trophoblasts are far outnumbered by the population of ce

33 ms through which excessive ER stress impacts trophoblasts are not well understood.

34 The ability to reverse trophoblast-associated inflammation with Rosiglitazone o

35 During pregnancy, placental trophoblasts at the feto-maternal interface produce a br

36 is a pleiotropic neuropeptide synthetized in trophoblasts at the maternal-placental interface.

37 By controlling trophoblast ATP production, mTORC1 links nutrient and O(

38 o secretions from the placenta or from model trophoblast barriers that had been exposed to altered ox

39 ependent entry pathway of virus infection in trophoblasts, but not in fibroblasts, highlighting the c

40 d that ALPPL2 is expressed only on placental trophoblasts, but not on any other normal tissues.

41 nists and can induce BCRP in human placental trophoblasts by activating AhR.

42 ssion of Hif-1alpha, explicitly in placental trophoblasts causes maternal pathology and establishes a

43 Unique to infected WIS rats, was loss of trophoblast cell density within the junctional zone of t

44 but no plac1 expression, demonstrating that trophoblast cell EVs express syncytin-1 on their surface

45 owever, the regulatory mechanisms that guide trophoblast cell fate decisions during placenta developm

46 olecular mechanism by which folate regulates trophoblast cell function.

47 , it also directly represses genes promoting trophoblast cell fusion.

48 se data demonstrate that BPA exposure alters trophoblast cell invasion and causes abnormal placental

49 rinted GelMA-based models to investigate the trophoblast cell invasion phenomenon, enabling studies o

50 ess in the transformed human first trimester trophoblast cell line (HTR-8/SVneo).

51 Using the human trophoblast cell line BeWo we have shown that low oxygen

52 ed the addition of small quantities of JEG-3 trophoblast cell line cells into clinical samples from s

53 -ring model) was tested with the HTR-8/SVneo trophoblast cell line to measure cell movement under the

54 d against HR-induced oxidative stress in the trophoblast cell line.

55 aluronic acid (HA), and sialic acid on human trophoblast cell lines and anchoring villous explants fr

56 In human trophoblast cell lines, we show SUPYN alters ASCT2 glyco

57 an placental cultures and in mouse and human trophoblast cell lines.

58 ted ACTN4 and beta-catenin colocalization on trophoblast cell podosomes, and ACTN4 down-regulation su

59 e inhibitor, GW2580, abolishes CSF-1 induced trophoblast cell proliferation and migration and can be

60 eover, knockdown of ACTN4 markedly inhibited trophoblast cell proliferation by reducing AKT membrane

61 nes, induction of apoptosis and reduction in trophoblast cell proliferation.

62 PBFS exposure altered trophoblast cell proliferation/invasion which might be m

63 monoclonal antibody, which targets the human trophoblast cell-surface antigen 2 (Trop-2), with SN-38,

64 Human trophoblast cell-surface marker (Trop-2) is a surface gl

65 hesized VIP as a critical factor in vivo for trophoblast-cell function and immune homeostasis mainten

66 the cell-cell interactome of fetal placental trophoblast cells and maternal endometrial stromal cells

67 It regulates the function of trophoblast cells and their interaction with decidual le

68 the population of differentiating, invasive trophoblast cells and, at least in mice, to the inductio

69 Placental trophoblast cells are potentially at risk from circulati

70 7 axis regulates genes in immortalized human trophoblast cells by targeting the ARID3B-complex.

71 ation of let-7 targets in immortalized human trophoblast cells by the ARID3B-complex.

72 Trophoblast cells differentiate into an invasive phenoty

73 ify enrichment and pick individual JEG-3 and trophoblast cells free of cervical cells.

74 We have developed a method to enrich trophoblast cells from a cervical sample using different

75 Isolation and in vitro culture of Sca-1(+) trophoblast cells from both differentiated TS cell cultu

76 recently, it has been impossible to isolate trophoblast cells from the human placenta that prolifera

77 profiled the transcriptome of 476 individual trophoblast cells from these conceptuses.

78 nvolved in the survival and proliferation of trophoblast cells in EP.

79 ppreciated that genetic analysis of fetal or trophoblast cells in maternal blood could revolutionize

80 ation and invasion, and invasion by isolated trophoblast cells in primary culture were significantly

81 es and show that they closely resemble human trophoblast cells in vivo.

82 ep of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophobl

83 We propose that mTOR folate sensing in trophoblast cells matches placental nutrient transport,

84 Abnormal functioning of trophoblast cells may cause failure of uterine spiral ar

85 nd LIGHT and sFlt-1 were co-localized in the trophoblast cells of HM.

86 results indicated that elevated LIGHT in the trophoblast cells of hydatidiform mole induces sFlt-1, w

87 s had a higher proportion of junctional zone trophoblast cells positive for cytoplasmic high temperat

88 from pregnant women or conditioned medium of trophoblast cells promoted endometrium receptivity in vi

89 sults were fully recapitulated by subjecting trophoblast cells to repetitive hypoxia-reoxygenation an

90 tus by infusion of granulysin into placental trophoblast cells via nanotubes, thus removing the intra

91 ation by DISCII antibodies on epithelial and trophoblast cells was similar to that in sera from wild-

92 When two or more high-quality trophoblast cells were available for singleton pregnanci

93 ment and function as well as interactions of trophoblast cells with the local and systemic maternal e

94 translocation of lysosomes to the surface of trophoblast cells, and inhibited lysosomal exocytosis, w

95 ormal maternal background with VIP-deficient trophoblast cells, here we demonstrate that trophoblast

96 anscriptional and epigenomic signatures with trophoblast cells, it has been proposed that the naive s

97 rtantly, PDGFRA was absent in epithelial and trophoblast cells, which were dependent upon the viral P

98 of proliferation, invasion, and migration of trophoblast cells.

99 esulting in inhibition of autophagic flux in trophoblast cells.

100 LIGHT directly induced sFlt-1 expression in trophoblast cells.

101 lization have their counterpart expressed in trophoblast cells.

102 pression in human placenta explants and JEG3 trophoblast cells.

103 proliferation by promoting PL expression in trophoblast cells.

104 gand (CSF-1) in immortalised first trimester trophoblast cells.

105 cells in the sample, making isolation of the trophoblasts challenging.

106 edominant paralog expressed in primary human trophoblast cultures.

107 n specific domains of DLX3 and GCM1 in human trophoblast-derived cells by performing immunoprecipitat

108 We hypothesized that trophoblast-derived hCG modulates the immune population

109 of early mechanisms that govern normal human trophoblast development and associated pathologies.

110 However, the mechanism controlling trophoblast development and differentiation during peri-

111 ro platform for future assessment of primate trophoblast development and function.

112 )-mA is essential for gene regulation during trophoblast development in cell culture models and in vi

113 enetic networks regulating peri-implantation trophoblast development.

114 valuable resource to study the regulation of trophoblasts development and differentiation during huma

115 Lastly, markers of trophoblast differentiation and invasion reverted to con

116 thesized that LIN28A and/or LIN28B regulates trophoblast differentiation and invasion, and that its d

117 creased LIN28B in preeclampsia impairs human trophoblast differentiation and migration.

118 unique epigenetic environment contributes to trophoblast differentiation and placenta formation.

119 While determining when trophoblast differentiation happens, our bioinformatic a

120 se, but the direct molecular consequences on trophoblast differentiation have not been investigated.

121 The function of TBX3 in trophoblast differentiation is then validated by a loss-

122 APA change is observed in multiple in vitro trophoblast differentiation models, and in single cells

123 LPS significantly reduced expression of the trophoblast differentiation proteins GCM1 and beta-hCG,

124 negative effect was accompanied by impaired trophoblast differentiation, increased glycogen accumula

125 been identified as an important molecule in trophoblast differentiation, suggesting its potential ro

126 diating a crosstalk between inflammation and trophoblast differentiation.

127 has been implicated as a major regulator of trophoblast differentiation.

128 sociated with both inflammation and abnormal trophoblast differentiation.

129 pressed in this organ and upregulated during trophoblast differentiation.

130 hat progesterone can regulate both timing of trophoblast elongation and DKK1 expression, DKK1 may be

131 ryonic development and hasten the process of trophoblast elongation around day 14-15 of pregnancy, wh

132 Trophoblast elongation occurred on day 14 in wild-type (

133 blastocyst stage embryo to modify subsequent trophoblast elongation.

134 ous adaptation and modifications between the trophoblast (embryonic) and the decidua (maternal).

135 ion between gametes, myoblasts, macrophages, trophoblasts, epithelial, cancer, and other cells in nor

136 le in the maintenance of the human placental trophoblast epithelium.

137 ntation, consequent on aberrant extravillous trophoblast (EVT) cell function during placental develop

138 o syncytiotrophoblast (SCT) and extravillous trophoblast (EVT) was a two-dimensional (2D) culture sys

139 pregnancy, semiallogeneic fetal extravillous trophoblasts (EVT) invade the uterine mucosa without bei

140 ring pregnancy, invading HLA-G+ extravillous trophoblasts (EVT) play a key role in placental developm

141 ternal cells and invading fetal extravillous trophoblasts (EVT).

142 in floating chorionic villi or extravillous trophoblasts (EVTs) at the anchoring villi.

143 Extravillous trophoblasts (EVTs) have the potential to provide the en

144 Extravillous trophoblasts (EVTs) were derived that express macaque EV

145 cated by invasive trophoblasts (extravillous trophoblasts (EVTs)) during early placentation.

146 hey differentiate into invasive extravillous trophoblasts (EVTs).

147 being permissive for ZIKV infection, primary trophoblasts expressed multiple putative ZIKV cell entry

148 TDC-derived CSF-2, acting via trophoblast-expressed CSFR2, contributes to thrombin-ind

149 l invasion, processes replicated by invasive trophoblasts (extravillous trophoblasts (EVTs)) during e

150 es to orchestrate stem versus differentiated trophoblast fate.

151 Here, we describe a protocol to isolate trophoblast from first-trimester human placentas that ca

152 d cost-effective method for enriching native trophoblasts from cervical samples for use in subsequent

153 study, we show that primary human placental trophoblasts from non-exposed donors (n = 20) can be inf

154 our data indicate that ACNT4 plays a role in trophoblast function and is required for normal placenta

155 nstrate that trophoblast VIP is critical for trophoblast function: VIP gene haploinsufficiency result

156 erall, our data indicate that IFITMs inhibit trophoblast fusion and suggest that there may be a criti

157 imp1-dependent regulatory networks governing trophoblast gene expression.

158 a occupied by spongiotrophoblast relative to trophoblast giant cells (GCs) within the junctional zone

159 Although SRC-3 expression in mouse trophoblast giant cells has been documented, its role in

160 t placentas exhibit an expansion of parietal trophoblast giant cells with a concomitant decrease in t

161 onses against a tumor antigen, 5T4 oncofetal trophoblast glycoprotein (5T4), which have been associat

162 leucine-rich repeat (LRR) adhesion protein, trophoblast glycoprotein (TPBG), as a novel PKCalpha-dep

163 mbryos may be due in part to enhancements of trophoblast growth and antiluteolytic signaling through

164 Further, at E19.5 labyrinth trophoblast had reduced glucose transporter 1 (GLUT1) an

165 Characteristic trophoblast hallmarks were defined in TSCs and ST includ

166 r before a protective zone of mature villous trophoblast has been established.

167 nd natural killer (NK) cells are involved in trophoblast immunosurveillance.

168 ere that prevention of the loss of the polar trophoblast in cattle results in ectopic domains of the

169 While loss of the persistent polar trophoblast in mice leads to reduced induction of gastru

170 tion of more severe iron deficiency in human trophoblast in vitro resulted in the regulation of both

171 a pro-invasive autocrine/paracrine factor in trophoblast in vitro.

172 ilure was caused by complement activation on trophoblasts in Cmas-/- implants and was accompanied by

173 R stress essentially disrupts homeostasis in trophoblasts in conjunction with autophagy inhibition by

174 ysis, PZP is found primarily in extravillous trophoblasts in the placenta.

175 ofiles of term intravillous and extravillous trophoblasts, including the transcriptome of the multinu

176 Conversely, stable IFITM knockdowns in BeWo trophoblasts increased their spontaneous fusion and allo

177 These data suggest that trophoblast infection may be a mechanism of transplacent

178 tide 3-kinase p110alpha in the fetus and the trophoblast interplay to regulate placental nutrient sup

179 The process of implantation, trophoblast invasion and placentation demand continuous

180 aternal morbidity, characterized by impaired trophoblast invasion and spiral artery transformation re

181 sed LIN28B may play a role in PE by reducing trophoblast invasion and syncytialization, and by promot

182 a practical tool for not only measurement of trophoblast invasion but also the interaction of invadin

183 mentary approaches, including HUVEC-mediated trophoblast invasion in nude mice, in vitro three-dimens

184 blishment of the correct cellular milieu and trophoblast invasion, all of which involve the action of

185 Insufficient trophoblast invasion, inadequate vascular remodeling, an

186 First trimester dNK facilitate trophoblast invasion, provide protection against infecti

187 itor), revealing a new role for NF-kappaB in trophoblast invasion.

188 preeclampsia which can result from aberrant trophoblasts invasion and subsequent placental ischemia.

189 owth factor (PlGF), abundantly produced from trophoblasts is involved in placental angiogenesis.

190 Using newly-optimized trophoblast isolation protocols that allow tracking of e

191 al to the domain of differentiation of these trophoblast-like cells; however, neither WNT nor NODAL f

192 We exposed a human trophoblast line, HTR8/SVneo, to PFBS.

193 n the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed u

194 modulated by biotin transporter activity and trophoblast mediated retention, and were in congruence w

195 Deletion of Ccdc8 in mice impaired trophoblast migration and placental development, resulti

196 Placental ischemia could impair trophoblast mitochondrial function and energy production

197 The molecular mechanisms regulating trophoblast mitochondrial oxidative phosphorylation are

198 ases, we identified on average 0.20 putative trophoblasts/mL, of which 55% were of high quality and s

199 blished an in vitro invasion-differentiation trophoblast model.

200 itutively active Hif-1alpha, specifically in trophoblasts, on mouse placental development in vivo.

201 Using cultures of human trophoblasts or mouse cells, we show that IFN-induced tr

202 nfirmed that there is similarity between the trophoblast organoids and in vivo placentas in their tra

203 Trophoblast organoids can be established within 2-3 week

204 The structural organization of these human trophoblast organoids closely resembles the villous plac

205 f the medium leads to differentiation of the trophoblast organoids into HLA-G+ EVT cells which rapidl

206 contain a single nucleus, cell types such as trophoblasts, osteoclasts, and skeletal myofibers requir

207 The polar trophoblast overlays the epiblast in eutherian mammals a

208 Trophoblast oxidative phosphorylation provides energy fo

209 Loss of trophoblast p110alpha resulted in viable fetuses, abnorm

210 note that, in all species in which the polar trophoblast persists, including humans and mice, ectopic

211 2 activation) in cultured term primary human trophoblast (PHT) cells.

212 unctions as a folate sensor in primary human trophoblast (PHT) cells.

213 d POA synthesis are reduced in primary human trophoblasts (PHTs) isolated from pregnancies complicate

214 ects of LPS on both extravillous and villous trophoblast physiology, and the involvement of the trans

215 nique patterns of expression among different trophoblast populations in first trimester placenta.

216 Here we examined the trophoblast potential of isogenic naive and primed hPSCs

217 drial function and sFLT1 production, a human trophoblast primary cell culture model was established i

218 MATERIALS AND Human trophoblast progenitor cells were isolated at 7-14 wk of

219 lar mechanisms that regulate self-renewal of trophoblast progenitors and their association with early

220 ic redundancy of Gata3 with paralog Gata2 in trophoblast progenitors ensures the successful progressi

221 Impairment of LSD1 function in trophoblast progenitors inhibits induction of endogenous

222 by controlling self-renewal and stemness of trophoblast progenitors within the placenta primordium.

223 educed Epcam expression (marker of labyrinth trophoblast progenitors), altered maternal blood space,

224 In trophoblast progenitors, GATA factors directly regulate

225 K4me3, H3K27me3, and CpG methylation maps of trophoblast progenitors, purified using the surface mark

226 tudy, we investigated the effects of PFBS on trophoblasts proliferation/invasion and signaling pathwa

227 acrine signaling via its receptor (CSF2R) in trophoblasts, promoting fetal membrane weakening and abr

228 c to this vesicle type, CD9 and HRS, and the trophoblast proteins placental alkaline phosphatase and

229 phoblast syncytialization via binding to the trophoblast receptor for syncytin-1, ASCT2, and hypothes

230 er either develop into invasive extravillous trophoblasts, remodeling the uterine vasculature, or fus

231 YAP-5SA with YAP KO cells and syncytializing trophoblasts revealed common target genes involved in tr

232 Stage-specific gene deletion in trophoblasts reveals that loss of both GATA genes, but n

233 mplemented a protocol for single circulating trophoblast (SCT) testing using positive selection by ma

234 However, key regulatory factors controlling trophoblast self-renewal and differentiation have been p

235 During later stages of pregnancy, placental trophoblasts serve as the major source of progesterone,

236 ts, including humans and mice, ectopic polar trophoblast signaling is prevented via epiblast cavitati

237 CN is physiologically expressed in placental trophoblasts, skeletal and hearth muscle, and kidney and

238 provides genetic evidence that impairment of trophoblast-specific GATA2/GATA3 function could lead to

239 d TFAP2A indicated that they directly couple trophoblast-specific gene induction with suppression of

240 earch indicates that prolonged expression of trophoblast-specific Hif-1alpha leads to a significant d

241 Male, but not female, mice with placental trophoblast-specific InsR deficiency showed a significan

242 An antiviral response was not evident in rat trophoblast stem (TS) cells following exposure to PolyI:

243 Trophoblast stem (TS) cells in the mouse derive from the

244 From these early embryo cells, trophoblast stem (TS) cells, embryonic stem (ES) cells a

245 CDX2 directly, we performed CDX2 ChIP-Seq on trophoblast stem (TS) cells.

246 Through embryonic stem (ES) to trophoblast stem (TS)-like cell reprogramming by introdu

247 se embryo, TEAD4 is selectively expressed in trophoblast stem cell-like progenitor cells (TSPCs), and

248 naive hPSCs can directly give rise to human trophoblast stem cells (hTSCs) and undergo further diffe

249 ishing idiopathic RPL patient-specific human trophoblast stem cells (RPL-TSCs), we show that loss of

250 ed by combining embryonic stem cells (ESCs), trophoblast stem cells (TS), and extra-embryonic endoder

251 opment, here we map super-enhancers (SEs) in trophoblast stem cells (TSCs) as a model.

252 Our objective was to develop macaque trophoblast stem cells (TSCs) as an in vitro platform fo

253 Trophoblast stem cells (TSCs) give rise to specialized c

254 bryonic stem cells (ESCs) and extraembryonic trophoblast stem cells (TSCs) in a three-dimensional sca

255 coculturing embryonic stem cells (ESCs) and trophoblast stem cells (TSCs) recapitulates this process

256 Induced trophoblast stem cells are molecularly and functionally

257 are molecularly and functionally similar to trophoblast stem cells derived from human blastocysts or

258 vivo mouse model and in vitro-derived murine trophoblast stem cells have been invaluable research too

259 cience that 3D co-cultures of mouse ESCs and trophoblast stem cells self-organize into embryo-like st

260 ent conditions (EPSCs) can be partnered with trophoblast stem cells to self-organize into blastocyst-

261 ther with recent successes in deriving human trophoblast stem cells, open up new and exciting prospec

262 upregulated during the development of mouse trophoblast stem cells, specifically at regions of stres

263 We report that in mouse trophoblast stem cells, the Airn and Kcnq1ot1 lncRNAs in

264 Using human trophoblast stem cells, we show that this phenotype can

265 or roles as enhancers in mouse embryonic and trophoblast stem cells.

266 reprogramming of somatic cells into induced trophoblast stem cells.

267 two-dimensional (2D) culture system of human trophoblast stem cells.

268 red, which enabled the derivation of induced trophoblast stem cells.

269 Importantly, trophoblast stem-cell-like cells can be generated from b

270 sts revealed common target genes involved in trophoblast stemness and differentiation.

271 arkers of both junctional zone and labyrinth trophoblast subtypes in a manner comparable to establish

272 PYN localization in villous and extravillous trophoblast subtypes, the decidua and even in placental

273 2-dimensional lattice formed by annexin V on trophoblast surfaces by anticardiolipin, via its interac

274 vely regulates the cell fusion essential for trophoblast syncytialization via binding to the trophobl

275 novel LSD1-GATA2 axis, which regulates human trophoblast syncytialization.

276 ncoding fusogenic proteins critical to human trophoblast syncytialization.

277 Our results support the relevance of trophoblast-synthesized VIP as a critical factor in vivo

278 These iPSCs were then converted to placental trophoblast (TB) representative of early pregnancy.

279 ne the transcriptomic landscape of placental trophoblast (TB) that surrounds the epiblast and associa

280 ntified genes downstream of p110alpha in the trophoblast that are important in adapting placental phe

281 The first in vitro model system of human trophoblast that could be cultured long term and differe

282 embryos display a hypo-proliferation of the trophoblast, the tissue that forms the placenta.

283 pitulate the antiviral properties of primary trophoblasts through the constitutive release of type II

284 s, C4BPA, binds to CD40 of placental villous trophoblast to activate p100 processing to p52, and in t

285 ly transfer it via nanotubes to extravillous trophoblasts to kill intracellular Listeria monocytogene

286 to non-fibroblast cells, including placental trophoblasts, to enable cCMV.

287 he PC is necessary for GPCMV epithelial cell/trophoblast tropism and congenital infection and is a po

288 Multipotent trophoblasts undergo dynamic morphological movement and

289 , there was complete concordance between all trophoblasts unless there was evidence of confined place

290 Fusion of placental trophoblasts via expression of endogenous retroviral fus

291 Trophoblast VIP deficiency entails immune homeostasis lo

292 trophoblast cells, here we demonstrate that trophoblast VIP is critical for trophoblast function: VI

293 expression in the three germ layers and the trophoblast was abnormal in the EBs of tetraploid ESCs c

294 orted populations of primary first-trimester trophoblasts, we evaluated the first stage of EVT differ

295 for the galectins expressed in extravillous trophoblast were validated in solid phase assays using r

296 In addition, cultured human trophoblasts were incubated with (13)C-cholecalciferol t

297 ly, MR766 is highly trophic toward primitive trophoblast, which may put the early conceptus of an inf

298 TM1, -2, and -3 also blocked fusion of these trophoblasts while making them more resistant to virus i

299 nd that it was also expressed in a subset of trophoblast within the chorion and labyrinth layer of th

300 -FLR strain can replicate in human placental trophoblasts without host cell destruction, thereby serv