ライフサイエンスコーパス: placental

1 gly support the primary source of PlGF to be placental.

2 s identified molecular mechanisms that limit placental ability to upregulate iron transport in the se

3 ure is the major factor contributing to most placental abnormalities and should therefore be targeted

4 enta weight ratios, and greater incidence of placental abnormalities relative to controls.

5 ID-19 complicated by severe preeclampsia and placental abruption.METHODSWe analyzed the placenta for

6 high fat diet significantly increased mouse placental abundance of PGC-1alpha expression and downstr

7 This placental adaptation that prioritizes placental iron is

8 development, an incomplete understanding of placental adaptation to limited iron availability has hi

9 Utilizing a pharmacologic approach to reduce placental adenosine levels, we found that enhanced adeno

10 Recent evidence indicates that elevated placental adenosine signaling contributes to preeclampsi

11 molecular basis for the chronically enhanced placental adenosine signaling in PE remains unclear.

12 sed therapy targeting the malicious cycle of placental adenosine signaling may elicit therapeutic eff

13 IF-1alpha) is crucial for the enhancement of placental adenosine signaling.

14 Placental alkaline phosphatase also showed high expressi

15 e, CD9 and HRS, and the trophoblast proteins placental alkaline phosphatase and HLA-G.

16 ning sparse genetic labeling and whole-mount placental alkaline phosphatase histochemistry, we found

17 ion occurs in early pregnancy during nascent placental and embryo development.

18 of detrimental maternal immune responses to placental and fetal antigens.

19 intrauterine growth restriction, evidence of placental and fetal brain hypoxia, and increased circula

20 Aneuploidies were detected in both placental and fetal compartments.

21 station, when pig placentae grow heavily, on placental and fetal development.

22 Placental and fetal Lm loads are lower and pregnancy suc

23 Following euthanasia of the pigs on d60, placental and fetal morphometry and biochemistry were me

24 u viruses, was found in acutely encephalitic placental and marsupial animals at a zoo in Germany and

25 ally methylated regions regulating germline, placental and tissue-specific transcription.

26 els and human placentas to explore maternal, placental, and fetal responses to alterations in iron st

27 regarding intertwin concordance of prenatal, placental, and infant outcomes.

28 se chain reaction (PCR) testing of maternal, placental, and neonatal samples was performed.

29 previously been associated with compromised placental antibody transfer, but the mechanism underlyin

30 lso probed in an in vitro model of the human placental barrier (polarized BeWo monolayers) using flow

31 l acids (PFAA) are repellants that cross the placental barrier, enabling interference with fetal prog

32 d fetal myeloid response or breakdown of the placental barrier.

33 Here, we review normal development of a placental bed with a safe and adequate blood supply and

34 by genetic variation potentially related to placental biology, and illustrate the utility of large-s

35 g peripheral and placental blood microscopy, placental blood loop-mediated isothermal amplification (

36 t delivery was detected using peripheral and placental blood microscopy, placental blood loop-mediate

37 n rooted in the maldevelopment of a maternal-placental blood supply capable of providing for the grow

38 Detection of the pathologic placental blood vessel lesion decidual vasculopathy (DV)

39 ponse to BPA/BPS exposure, likely affect the placental-brain axis of the developing mouse fetus.

40 o CD46 variants were associated with reduced placental CD46 expression and one CFH variant was associ

41 ngenital infections, are highly expressed by placental cell types.

42 intracellular pathogen without damage to the placental cell.

43 and the repair of spontaneous DNA damage in placental cells, suggesting that genotoxic stress and en

44 Placental chorioamniotic membranes were studied using RN

45 ty and leads to preterm premature rupture of placental chorioamniotic membranes.

46 , any compromise in the development of fetal-placental circulation significantly affects maternal-fet

47 itioning between the maternal, neonatal, and placental compartments were identified.

48 itioning between the maternal, neonatal, and placental compartments.

49 Placental complement deposition and maternal alternative

50 nule proteins, strongly inhibits Lm in human placental cultures and in mouse and human trophoblast ce

51 In humans, a subset of placental cytotrophoblasts (CTBs) invades the uterus and

52 This signalling capacity is skewed when placental damage occurs and can deliver a dangerous path

53 We establish a significant role for placental defects in the development of CdLS mouse embry

54 Placental DeltaR2* during maternal hyperoxia changed wit

55 Results Placental DeltaR2* increased during maternal hyperoxia i

56 s that will help deepen our understanding of placental development and associated disorders of pregna

57 we have conducted a longitudinal analysis of placental development and fetal growth using a mouse mod

58 s an experimental model to investigate human placental development and function as well as interactio

59 ingolipids have been implicated in mammalian placental development and function, but their regulation

60 s for gaining insights into these aspects of placental development and function, with recent studies

61 dels provide limited information about human placental development and function.

62 l growth restriction arise from disorders of placental development and have some shared mechanistic f

63 ll developmental potential and causes latent placental development and reduced fetal growth.

64 specialised functions dedicated to achieving placental development and successful reproduction.

65 These data profile placental development at an unprecedented resolution, pr

66 illous trophoblasts (EVT) play a key role in placental development, uterine spiral artery remodeling,

67 on fetal development, neonatal outcomes, and placental development.

68 hing is known about NPFF-NPFFR2 functions in placental development.

69 rify and culture primary HLA-G+ EVT from the placental disk and chorionic membrane from healthy term

70 Preeclampsia (PE) is a placental disorder with different phenotypic presentatio

71 erapies such as PlGF overexpression, to cure placental disorders during pregnancy.

72 iomarker for the diagnosis and management of placental disorders.

73 reveal that excessive placental DNA damage in murine models for Cornelia de La

74 al overgrowth, reduced fetal weight, reduced placental DNA methylation and increased levels of sFLT1,

75 Our results suggest that placental DNA methylation is fundamentally linked to the

76 ons between maternal insulin sensitivity and placental DNA methylation markers across the genome.

77 delivery, we identified 188 CpG sites where placental DNA methylation was associated with Matsuda in

78 megalin-targeting liposome nanocarriers for placental drug delivery.

79 nectin levels during late gestation reversed placental dysfunction and fetal overgrowth in a mouse mo

80 The contribution of ZIKV NS1 to placental dysfunction during ZIKV infection remains unkn

81 nsporter activity is part of the spectrum of placental dysfunction in FGR.

82 unction, the possible role of ferroptosis in placental dysfunction is largely unknown.

83 Rationale: Antenatal inflammation with placental dysfunction is strongly associated with high b

84 indings suggest that ZIKV NS1 contributes to placental dysfunction via modulation of glycosaminoglyca

85 e placenta, resulting in local inflammation, placental dysfunction, and, consequently, adverse pregna

86 Its pathophysiology involves placental dysfunction, but the mechanism is unclear.

87 ive stress and lipotoxicity are hallmarks of placental dysfunction, the possible role of ferroptosis

88 potentially dire consequences of generalized placental dysfunction.

89 First, BPS exposure causes almost identical placental effects as BPA.

90 1) placental weights and a lower (P = 0.013) placental efficiency (fetal/placental weight), although

91 nd inhibited maternal high fat diet-impaired placental efficiency and glucose tolerance in offspring.

92 between d40 to d60 of gestation reduced pig placental efficiency, resulting in compensatory growth o

93 bre number density and a thicker (P = 0.017) placental epithelial layer compared to their TN counterp

94 l profiling by mass spectrometry showed that placental EVs were enriched for proteins that function i

95 Metformin treatment on male diabetic placental explant activated AMPK and stimulated PGC-1alp

96 Effects of metformin were examined in human placental explants from a subgroup of diabetic women and

97 Finally, placental explants showed a significant increase in CORI

98 We found MNR to be associated with increased placental expression of FA binding and transport protein

99 al nutrient restriction, MNR) to investigate placental expression of FA transport and binding protein

100 nduced increases in IgG and increased FCGR3A placental expression.

101 We hypothesized that placental FA transport proteins (FATP) and FA binding pr

102 Placental FABP1 and FABP5 expression was increased in MN

103 However, little is known about placental fatty acid (FA) transport in IUGR.

104 Neither maternal systemic inflammation nor placental (fetal) inflammation was a feature of FGR in W

105 Neonatal PCR testing, placental findings, and infant outcomes can be discordan

106 amine and glutamate are essential for normal placental function and fetal development; whether transp

107 ial/ethnic differences in mutational load on placental function directly affecting offspring developm

108 and cAMP are known to play a central role in placental function, their regulation of STC-1 points to

109 Disrupted placental functioning due to stress can have lifelong im

110 (BMI) might share both peripheral blood and placental gene signatures that link these conditions tog

111 have used an integrated approach to discover placental genetic and epigenetic markers of preeclampsia

112 f how the immune system adapted to mammalian placental gestation and could be an important considerat

113 s to the adaptive immune system required for placental gestation.

114 thesised that FGR is associated with reduced placental glutamine and glutamate transporter activity a

115 ts, in vitro exposure to rapamycin inhibited placental glutamine and glutamate uptake (24 h, uncompli

116 how virus-induced inflammation impacts fetal-placental growth and developmental trajectories, particu

117 Placental growth factor (PlGF) is an angiogenic factor i

118 he plasma soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF) ratio.

119 r(7), the soluble fms-like tyrosine kinase 1:placental growth factor (sFLT1:PlGF) ratio (AUC 0.78 ver

120 e of this IAV-driven vascular storm included placental growth retardation and intrauterine growth res

121 and Dlk1, which encode proteins critical for placental growth.

122 No detectable changes in placental hemodynamics were observed, as determined by u

123 conditions or in iron deficiency, fetal and placental hepcidin did not regulate fetal iron endowment

124 Overall, we demonstrated that (a) elevated placental HIF-1alpha by AT(1) -AA or LIGHT upregulates C

125 ignaling through upregulated ADORA2B induces placental HIF-1alpha expression, which creates a positiv

126 that enhanced adenosine underlies increased placental HIF-1alpha in an angiotensin receptor type 1 r

127 Knockdown of placental HIF-1alpha in vivo suppressed the accumulation

128 Our findings suggest that placental histological changes and PM are independent ri

129 Alterations in placental histology are frequently reported in these pre

130 al chemistry, maternal liver histopathology, placental histopathology, embryo weight, placental weigh

131 ediated isothermal amplification (LAMP), and placental histopathology.

132 yl species (FeNOs), are relatively stable in placental homogenates from normal placentas, and that NO

133 species (FeNOs), are relatively unstable in placental homogenates from normal placentas.

134 stability and metabolic fate of NOx in human placental homogenates from uncomplicated pregnancies in

135 ous NO, nitrite and nitrosothiols react with placental homogenates to form iron nitrosyl complexes.

136 hat NO, nitrite and nitrosothiols react with placental homogenates to form iron nitrosyl complexes.

137 NOx have differential stability in placental homogenates.

138 ination of the stability of exogenous NOx in placental homogenates.

139 d only in the presence of monocytes, grew on placental hormones, remained viable within antigen prese

140 their transcriptomes and ability to produce placental hormones.

141 ance to human disease since dysregulation of placental Htra1 and placental oxidative stress are featu

142 Placental hypoxia in the RUPP was confirmed with histolo

143 that it may act to protect against prolonged placental hypoxia seen in preeclampsia.

144 reeclampsia processes in these models (e.g., placental hypoxia, immune dysfunction, angiogenesis, oxi

145 IFN-lambda1 is a key placental IFN that appeared less protective than IFN-alp

146 ansporter (GLUT-3) and increased (P = 0.037) placental IGF-2 mRNA expression.

147 Placental immune responses are highly regulated to strik

148 l controversial with some believing it to be placental in origin while others refute this.

149 KV I1404 increased the magnitude and rate of placental infection and conferred fetal infection, in co

150 e placentation, but how they protect against placental infection while maintaining fetal tolerance is

151 likely driven by declining susceptibility to placental infection.

152 Among 125 placental infections, A581G-bearing parasites were assoc

153 e of NO and NOx under conditions of aberrant placental inflammation during pregnancy.

154 ical relevance for studies aiming to prevent placental inflammatory disorders as well as maternal-to-

155 HLA-G+ EVT in the development of detrimental placental inflammatory responses associated with pregnan

156 ne vein (ipsilateral or contralateral to the placental insertion) during caesarean section and from a

157 ion have altered phenotypes, possibly due to placental insufficiency and impaired fetal growth.

158 Using a sheep model of placental insufficiency and IUGR, we have previously dem

159 Low circulating SPINT1 is a marker of placental insufficiency and may identify pregnancies wit

160 Placental insufficiency can cause fetal growth restricti

161 Placental insufficiency during early-mid gestation may h

162 sociation between low circulating SPINT1 and placental insufficiency in two other cohorts.

163 ling of the fetal circulation resulting from placental insufficiency is associated with more favourab

164 There are no reliable screening tests for placental insufficiency, especially near-term gestation

165 deficit in humans, and is commonly caused by placental insufficiency, which results in fetal hypoxia.

166 d and neonatal anthropomorphic indicators of placental insufficiency.

167 station and low birthweight, an indicator of placental insufficiency.

168 Among mammals, placental invasion is correlated with vulnerability to m

169 ot embryonic, hepcidin determined embryo and placental iron endowment in a healthy pregnancy.

170 regulate fetal iron endowment by controlling placental iron export.

171 d against any confounding effects of altered placental iron homeostasis, we generated fetuses with a

172 t FPN was surprisingly decreased to preserve placental iron in the face of fetal iron deficiency.

173 This placental adaptation that prioritizes placental iron is mediated by iron regulatory protein 1

174 deficiency, critical transporters mediating placental iron uptake (transferrin receptor 1 [TFR1]) an

175 berrant trophoblasts invasion and subsequent placental ischemia.

176 enhanced staining for ET-1 receptors in the placental labyrinthine zone in hypoxic compared to normo

177 It was reported that placental lactogen (PL) plays a crucial role in pregnanc

178 Transgenic expression of placental lactogen in beta-cells of Ak mice drastically

179 y in both the mother and fetus decreases the placental levels of sphingolipids, including sphingoid b

180 ed mechanistic insights into the ill-defined placental lipotoxicity that may inspire PLA2G6-targeted

181 The importance of fetal placental macrophages (Hofbauer cell [HCs]) is underscor

182 eficiency and explored a potential marker of placental maladaptation.

183 after delivery for pathological lesions and placental malaria (PM).

184 t (primary outcome) attributed to preventing placental malaria infection (mediator).

185 difference 69 g, 95% CI 26 to 112), despite placental malaria infection being lower in the dihydroar

186 Placental malaria infection complicates one quarter of a

187 Placental malaria was 64 (48.1%) and 21 (15.8%) respecti

188 ing novel strategies to prevent and/or treat placental malaria.

189 VAR2CSA is the placental-malaria-specific member of the antigenically v

190 mammals and the corpus callosum is unique to placental mammals (eutherians).

191 X-chromosome dosage compensation in female placental mammals is achieved by X-chromosome inactivati

192 rehensive tRNA gene ortholog set spanning 29 placental mammals to estimate the evolutionary rate of f

193 Although EZHIP is not found outside placental mammals, expression of human EZHIP reduces H3K

194 ngation of CA1 is also present in some other placental mammals, notably the elephant shrew, hyrax, ca

195 evolved simultaneously upon the emergence of placental mammals, suggesting that PD-L2-affinity tuning

196 n piRNA genes are syntenic to those in other placental mammals, their sequences are poorly conserved.

197 rsification of short histone H2A variants in placental mammals.

198 sed short histone H2A variants that arose in placental mammals.

199 tivation of an entire X chromosome in female placental mammals.

200 e mammalian POLG gene, which became fixed in placental mammals.

201 n referred to as ORF-Y that arose de novo in placental mammals.

202 cleavage-specific transcriptional program in placental mammals.

203 In eutherian (placental) mammals, brown adipose tissue (BAT) can also

204 sought to perform an objective comparison of placental microscopic appearance in normal and complicat

205 est the capability of metformin to stimulate placental mitochondrial biogenesis and inhibit the aberr

206 ciation between maternal lifetime stress and placental mitochondrial DNA mutational load in an urban

207 odel maternal lifetime stress in relation to placental mitochondrial DNA mutational load.

208 nments, such as diabetes and obesity, impair placental mitochondrial function, which affects fetal de

209 lifetime exhibited a higher number of total placental mitochondrial mutations (beta = .23, 95% confi

210 luorescence probe was assessed in an in vivo placental model - timed-pregnant Balb/c mice at gestatio

211 report advance the use of the 3D bioprinted placental model as a practical tool for not only measure

212 nness centrality in the peripheral blood and placental modules.

213 At the maternal-fetal interface, density of placental mononuclear leukocytes decreased with stress,

214 avid women suspected of having PAS underwent placental MRI as part of a prospective trial.

215 Elevated temperatures decreased (P = 0.026) placental mRNA expression of a glucose transporter (GLUT

216 g expression of C19MC miRNAs and the macaque placental nonclassical MHC class I molecule, Mamu-AG.

217 We hypothesized that placental NOx would be increased in FGR vs. normal tissu

218 vels of soluble CORIN in preeclampsia have a placental origin.

219 exhibit this compensation but rather display placental overgrowth, reduced fetal weight, reduced plac

220 While placental oxidative stress and lipotoxicity are hallmark

221 e since dysregulation of placental Htra1 and placental oxidative stress are features of preeclamptic

222 Six minutes of maternal hyperoxia increased placental oxygenation in healthy fetuses and fetuses wit

223 Placental pathological abnormalities are more frequently

224 with T-cell infiltration of the placenta and placental pathological abnormalities.

225 n those with no obstruction to have abnormal placental pathology (79% vs. 44%).

226 Further multivariate analyses showed placental pathology (adjusted (aOR) 3.0, 95% CI = 1.2-7.

227 However, the relationship between placental pathology and Plasmodium falciparum infection

228 Preeclampsia is the most common placental pathology in pregnant females, with increased

229 The presence of placental pathology increased the risk of PE, with parti

230 ryonic lethality around mid-gestation due to placental pathology that involves severe disruption to s

231 en with PAS (86%) and in 67 of 68 women with placental percreta (98%).

232 PAS was diagnosed in 126 of 155 women (81%) (placental percreta in 68 of 126 [54%]).

233 PAS and 10 (95% CI: 1.5, 70.4; P < .001) for placental percreta when IFVs were visible.

234 both female and male fetuses but affects the placental phenotype sex-specifically.

235 outer cells initiating a trophectoderm (TE) placental progenitor program.

236 (14)C-glutamine and (14)C-glutamate (per mg placental protein) but higher expression of key transpor

237 specific chondroitin-4-sulfate chains of the placental proteoglycan receptor.

238 d a new physiological phenomenon, the 'utero-placental pump', by which the placenta and underlying ut

239 is using RNA sequencing metagenomics(4-6) of placental samples from normal and complicated pregnancie

240 hemicals until embryonic day 12.5, whereupon placental samples were collected and compared with unexp

241 Plasma and placental samples were collected at GD120 (control n = 8

242 r miscarriage in association with documented placental SARS-CoV-2 infection.

243 nant women with AMSB underwent a 21-24 week "placental screen" comprising fetal and placental size, a

244 Placental screening effectively identified early-onset (

245 We discuss the placental secretome including glycoproteins, microRNAs a

246 suggesting that genotoxic stress and ensuing placental senescence and cytokine production could repre

247 within the junctional zone, markedly reduced placental serotonin (5-HT) concentrations, and lowered 5

248 week "placental screen" comprising fetal and placental size, and uterine artery Doppler.

249 ive fetuses and abortions, and no changes in placental size.

250 n with AMSB and test the predictive value of placental sonographic screening to predict early-onset F

251 hypervascularity, and signs of extrauterine placental spread).

252 comitant with smaller placentas, and altered placental structure at midgestation.

253 ure and function, prevents RVH, and improves placental structure following antenatal ETX exposure.

254 lity, and may be due to excessive release of placental syncytiotrophoblast-derived extracellular vesi

255 Placental syncytiotrophoblasts at the maternal-fetal int

256 Furthermore, confocal images of placental SynT cross-sections show a 3-fold increase of

257 hown in earlier studies, and used to prepare placental-targeting liposomes.

258 tal weight, internal chemical dosimetry, and placental thyroid hormone levels were determined.

259 glycoprotein originally identified in human placental tissue and subsequently found to be highly exp

260 bortion, at which time the pathogen titer in placental tissue can exceed one billion bacteria per gra

261 ncies in healthy mothers compared to that in placental tissue from normotensive and pre-eclamptic pre

262 profiles in maternal plasma might serve as a placental tissue specific biomarker for preeclampsia.

263 alysis of season of birth in full-term human placental tissue to evaluate whether the placenta may be

264 in maternal blood, umbilical cord blood, and placental tissue when available.

265 STC-1 protein expression in first trimester placental tissue.

266 n of any associated therapeutic cargo in the placental tissue.

267 family that act from the carpel wall and the placental tissue.

268 osomes (intercellular junctions) was seen in placental tissues from women with pPROM.

269 , comparing infected human nasal mucosal and placental tissues, representing the viral entry and the

270 ay thus have independent effects on fetal or placental tissues.

271 r approximately 11.9% of all 17 664 analyzed placental transcripts.

272 gnificant amount of observed variance in net placental transfer of absorbed iron (R = 0.95, P = 0.03)

273 ay act as reservoirs for trimester-dependent placental transmission of ZIKV, accounting for the highe

274 IUGR) is associated with specific changes in placental transport of amino acids, folate and ions.

275 ies) indicating a role of mTOR in regulating placental transport of these amino acids.

276 riction with data that suggest adaptation of placental transport to maintain delivery of critically n

277 These data suggest the adaptation of placental transport when aiming to maintain delivery of

278 Placental trophoblast cells are potentially at risk from

279 eloping fetus by infusion of granulysin into placental trophoblast cells via nanotubes, thus removing

280 pivotal role in the maintenance of the human placental trophoblast epithelium.

281 During later stages of pregnancy, placental trophoblasts serve as the major source of prog

282 ssues found that ALPPL2 is expressed only on placental trophoblasts, but not on any other normal tiss

283 rom failures in the differentiation of human placental trophoblasts.

284 est that ACER2 sustains the integrity of the placental vasculature by controlling the homeostasis of

285 key role in sustaining the integrity of the placental vasculature by regulating the homeostasis of s

286 ated by isolating first and second trimester placental villous cytotrophoblasts followed by culture i

287 Human in vitro studies using placental villous explants demonstrated that increased H

288 Placental villous tissue (n = 823) and edge biopsies (n

289 NOx levels in placental villous tissue are increased in fetal growth r

290 Furthermore, NOx levels in placental villous tissue are increased in FGR vs. placen

291 Infiltration of CD8(+) T-cells into the placental villous tissue occurred in both fetal growth r

292 wledge gap, we used scRNA-seq to profile the placental villous tree, basal plate, and chorioamniotic

293 f these 48 proteins, C4BPA, binds to CD40 of placental villous trophoblast to activate p100 processin

294 multiple birth; pre-delivery LoS >= 3 days; placental weight >= 600 g; maternal age 40-44 years; >=6

295 were more likely with gestation >= 41 weeks, placental weight <500 g and especially labour analgesia.

296 sia/pre-eclampsia; maternal age 40-44 years; placental weight 600-99 g; oligohydramios; pre-delivery

297 ower (P = 0.013) placental efficiency (fetal/placental weight), although fetal weights were not signi

298 gy, placental histopathology, embryo weight, placental weight, internal chemical dosimetry, and place

299 etuses, ET fetuses had increased (P = 0.041) placental weights and a lower (P = 0.013) placental effi

300 hts, changes in liver histopathology, higher placental weights and embryo-placenta weight ratios, and