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1 ce in angiogenic growth factors and abnormal placentation.
2 NK-trophoblast interactions may lead to poor placentation.
3 is required for successful implantation and placentation.
4 reproduction scheme involving viviparity and placentation.
5 e decidua are important regulators of normal placentation.
6 ng KIR on maternal dNK may be beneficial for placentation.
7 in that have been captured for a function in placentation.
8 roductive character in apes, highly invasive placentation.
9 estigation of the involvement of NK cells in placentation.
10 iron metabolism is associated with defective placentation.
11 stablishing an experimental model of primate placentation.
12 stemic inflammatory state as well as shallow placentation.
13 theria species that have a different form of placentation.
14 to delineate hypoxia-sensitive events during placentation.
15 ion and those associated with aberrations of placentation.
16 Oxygen is a critical regulator of placentation.
17 zation, and embryonic PPARdelta is vital for placentation.
18 nsor to direct trophoblast cell fates during placentation.
19 maternal role of COUP-TFII in regulating the placentation.
20 emodeling of arterioles, a hallmark of human placentation.
21 irst step of implantation and, subsequently, placentation.
22 villous trophoblasts (EVTs) influences human placentation.
23 terine wall is characteristic of hemochorial placentation.
24 PAR2 and PAR3 in the invasive phase of human placentation.
25 regulates trophoblast invasion during early placentation.
26 giogenesis are hallmarks of implantation and placentation.
27 d permits the unique arrangement for primate placentation.
28 understanding factors that lead to abnormal placentation.
29 travillous trophoblasts (EVTs)) during early placentation.
30 ng neural tube closure, digit septation, and placentation.
31 vivo and that HIF is essential for mammalian placentation.
32 pivotal to understanding normal and abnormal placentation.
33 successful endovascular invasion and normal placentation.
34 blast cells currently exist for the study of placentation.
35 do not kill infected fetal cells but promote placentation.
36 tentially critical process in early ruminant placentation.
37 he progressive phases of decidualization and placentation.
38 ophoblast cell lineage development and human placentation.
39 ses, coopted for a physiological function in placentation.
40 ator of trophoblast fate choice during human placentation.
41 ue samples to determine how uNK cells affect placentation.
42 sential roles in trophoblast development and placentation.
43 leterious effects early in pregnancy, during placentation.
44 the BAP1 PR-DUB complex in regulating early placentation.
45 novel molecular node controlling early mouse placentation.
46 asion; features also characteristic of human placentation.
47 ards a crucial role for EP300 in early human placentation.
48 useful animal model for studying hemochorial placentation.
49 ed, likely allowed for an extended period of placentation.
50 mmals and is thought to have co-evolved with placentation.
51 rentiation is a conserved event during human placentation.
52 activity, reinforcing their critical role in placentation.
53 radiated with the evolution of haemochorial placentation.
54 may be associated with diseases of abnormal placentation.
55 racrine signals that govern implantation and placentation.
56 for understanding TE lineage development and placentation.
57 captured during evolution for a function in placentation.
58 first pregnancies, is associated with faulty placentation.
59 n between prenatal PFBS exposure and adverse placentation.
60 that allowed an extended period of intimate placentation.
61 kely critical during the beginning stages of placentation.
62 the first trimester, optimizing hemochorial placentation.
63 of the CEBP and GATA families essential for placentation.
64 tein dysregulation in EVT cells during early placentation.
65 he syncytialisation process is essential for placentation.
66 se, was unable to activate matriptase during placentation.
67 aptured by eutherian mammals, with a role in placentation.
68 tment of pregnancy loss mediated by abnormal placentation.
69 eclampsia, a syndrome arising from defective placentation.
70 FMVD regulation in normal and dysfunctional placentation.
71 ene that has evolved a function in eutherian placentation.
72 in that have been captured for a function in placentation.
73 in that have been captured for a function in placentation.
74 lated lineages in the presence or absence of placentation.
75 e imaging modalities for diagnosing abnormal placentation.
76 invasion is a fundamental component of human placentation.
77 ternal-fetal immune mechanism that regulates placentation.
78 igin, ancestrally captured for a function in placentation.
79 s morbidity increased in cases with abnormal placentation.
80 th placenta previa with and without abnormal placentation.
81 5]; n=235 021 women, nine studies), abnormal placentation (3.9% [0.1-7.6]; n=29 638 women, two studie
85 ary, maternal hypoxia during early stages of placentation activates the invasive endovascular trophob
86 e most significant risk factors for abnormal placentation, added to risk factors known for placenta p
87 found substantial variation in the degree of placentation among natural populations associated with p
88 estriction (FGR) is associated with aberrant placentation and accounts for a significant proportion o
89 show that the essential function of HAI-1 in placentation and all other embryonic processes is to res
91 ified as having USs exhibit epitheliochorial placentation and are in the Ruminantia and Suidae orders
93 e study can only represent a period of early placentation and clinical pregnancy loss during the seco
94 selective FOXO1 knockdown leads to defective placentation and compromised embryo development, similar
95 Colony stimulating factor-1 (CSF-1) promotes placentation and creates a pro-inflammatory environment
97 roup showing multiple independent origins of placentation and extreme variation in male sexually sele
101 scular modification are implicated in normal placentation and fetal growth in humans, our findings su
102 d in vivo prior to transfer can impair early placentation and fetal growth, but this effect normalize
103 addition to the role of uterine NK cells in placentation and fetal growth, other uterine ILCs (uILCs
104 molecular and genomic changes that underlie placentation and find that two distinct evolutionary mec
105 ble importance both for the study of healthy placentation and for the investigation of the potential
106 ntiation of trophoblasts and helps in normal placentation and formation of vascular exchange interfac
109 s is not a consistent feature of hemochorial placentation and has hindered the establishment of suita
110 etween maternal and fetal cells during early placentation and highlights novel avenues for research t
111 cations including low birth weight, abnormal placentation and increased risk for rare imprinting diso
112 rrations in embryo spacing, decidualization, placentation and intrauterine embryonic growth, manifest
113 cytotrophoblasts (CTBs) is vital for healthy placentation and is impaired in preeclamptic pregnancies
114 of decidualized endometrium is essential for placentation and is tightly regulated and involves troph
115 origin that have been co-opted for a role in placentation and likely contribute to the remarkable div
120 hat endocannabinoid signaling is critical to placentation and pregnancy success in humans and implica
124 pregnancy for species with epitheliochorial placentation and some but not all Laurasiatheria species
125 demonstrate both clade-specific patterns of placentation and specific cases of convergent evolution
129 n vivo evidence that IGFBP-1 plays a role in placentation and suggests that IGFBP-1 has a pathologica
131 ese complications have their origin in early placentation and that EP300 is involved in that process.
132 etween syndromic manifestations of defective placentation and the incidence of intellectual disabilit
133 ioxidant defenses may contribute to abnormal placentation and the later development of pregnancy comp
134 he current evidence for the role of abnormal placentation and the role of placental factors such as t
135 Given the role of imprinted genes in human placentation and the vulnerability of imprinted genes to
136 -induced adaptations critical to hemochorial placentation and thus nutrient flow to extraembryonic an
137 o modulate several processes associated with placentation and to promote maternal tolerance toward fe
140 e of the maternal microenvironment in normal placentation, and highlights potential pathways that can
141 t cell invasion, a feature shared with human placentation, and is also amenable to gene manipulation
142 normal placentation; however, TPbeta impairs placentation, and promotes the development of IUGR, and
145 encode a protein critical for vasodilation, placentation, and uterine expansion during pregnancy (lo
147 thrombosis (alphaIIbbeta3) and implantation, placentation, angiogenesis, bone remodeling, and tumor p
153 ates are excellent models for studying human placentation as experimental manipulations in vitro can
154 Maternal decidual NK (dNK) cells promote placentation, but how they protect against placental inf
155 cells (uNK) play a role in the regulation of placentation, but their functions in nonpregnant endomet
156 dds to our understanding of implantation and placentation by reporting the expression and function of
157 t had preterm birth associated with aberrant placentation (cases who had preeclampsia and/or intraute
158 cations associated with ischemia or abnormal placentation, CIs of aORs for SCD and anemia groups over
159 ulations had significantly higher degrees of placentation compared to low predation females, while nu
160 to the profound differences in pregnancy and placentation comparing humans and the most commonly used
161 Preeclampsia (PE) is characterized by poor placentation, consequent on aberrant extravillous tropho
164 s in mouse are caused by decidualisation and placentation defects that can be rescued by transferring
165 n aged female mice is associated with severe placentation defects, which result from major deficits i
166 ss of implantation, trophoblast invasion and placentation demand continuous adaptation and modificati
168 stem cells as a discovery platform for human placentation disorders and suggest that LIMK1 activity h
169 causal or pathogenetic model of superficial placentation driven by immune maladaptation, with subseq
170 echanisms and in turn sustaining hemochorial placentation during the long gestation of anthropoid pri
171 eaction is even involved in epitheliochorial placentation (e.g., pig), this study found no evidence o
172 mochorial species, characterized by invasive placentation, endometrial stromal fibroblasts (ESFs) und
176 of the anchoring villi convert during human placentation from a transporting epithelium to an invasi
177 all 115 conserved eutherian chorioallantoic placentation genes in the uterus, an XY(1)Y(2) sex chrom
182 During the second trimester of pregnancy, placentation has evolved to the point at which nutrients
184 epigenetic requirements that underpin normal placentation has remained remarkably under-appreciated.
185 Cyprinodontiformes, in which livebearing and placentation have evolved several times independently.
187 e that expression of TPalpha mediates normal placentation; however, TPbeta impairs placentation, and
189 n selection coincident with the evolution of placentation in fishes, with particularly strong selecti
191 ve been used for the convergent evolution of placentation in independently evolved and highly distant
195 iated with an increased risk of disorders of placentation in subsequent pregnancies, but effects on t
198 n the diagnostics and management of abnormal placentation in women with placenta previa and to compar
199 h critical contribution for implantation and placentation, including "in utero embryonic development,
200 lar program that is reminiscent of eutherian placentation, including both fetal and maternal signals.
206 s hypothesis, which is that the evolution of placentation is associated with reduced pre-copulatory f
207 with a noninvasive epitheliochorial type of placentation is critical establishing an adequate uterin
214 nclude that the evolution of highly invasive placentation is the outcome of both the evolution of inv
215 macropodids (wallabies and kangaroos), with placentation lasting beyond the 2 to 4 d seen in other m
218 nterrelated biological adaptations involving placentation, maternal immune responses, and hormonal ho
219 of selection pressures on the efficiency of placentation may stem from changes in nutritional demand
221 olves by arguing that an increased degree of placentation offers a selective advantage in high predat
222 ing to two selective optima, associated with placentation: one represented by small-bodied species th
224 pears to be an important component of normal placentation, perhaps limiting the proliferative and inv
225 renine during pregnancy can lead to impaired placentation, placental hypoperfusion, an antiangiogenic
227 elected traits (pre-copulatory), rather than placentation (post-copulatory), that are associated with
228 on, and cervical insufficiency) and abnormal placentation (preeclampsia and intrauterine growth restr
229 in endometrial cells, which is essential for placentation/pregnancy in eutherian mammals and is a dir
235 ns the most common cause of IUGR is impaired placentation resulting from poor trophoblast function, w
236 es of rabbit biology, including primate-type placentation, short gestation, and delivery of litters,
238 important compartment within the hemochorial placentation site that is essential for a healthy pregna
239 , leading to decreased oxygen tension at the placentation site, stabilized hypoxia-inducible factor 1
241 cental oxidative stress induced by defective placentation sits at the epicenter of the pathophysiolog
242 g post-natal lactation than during pre-natal placentation, so there may be greater selection for geno
243 those associated with ischemia and abnormal placentation, suggesting that prenatal anemia may be a m
245 ene family known to be involved in mammalian placentation: the prolactins (two clusters), serpins, ca
246 es, including the syncytins that function in placentation, there are examples of co-opted gag genes i
247 We conclude that NK cells guide hemochorial placentation through controlling a hypoxia-sensitive ada
248 nderstanding the pathophysiology of impaired placentation to establish screening tests for stillbirth
249 icated genes are utilized at later stages of placentation to meet the metabolic needs of a diverse ra
252 lantation, stromal cell decidualization, and placentation. Uterine gland dysfunction is considered a
254 ulating invasive trophoblast and hemochorial placentation was investigated using Rcho-1 trophoblast s
255 ence of histologic features of dysfunctional placentation, was associated with preeclampsia and fetal
256 le effects of the maternal genotype on fetal placentation, we generated transgenic mice that expresse
258 tion reflect the pathology of defective deep placentation, where conversion of uterine spiral arterie
259 the uterus during decidualization and early placentation, whereas ST2 is expressed by uterine immune
260 cipate in implantation, decidualization, and placentation, whether there is a common molecular link t
262 ncomplicated pregnancy and is present during placentation, which occurs under low oxygen tensions.
266 The clinical syndrome begins with abnormal placentation with subsequent release of antiangiogenic m
267 car disturbs stroma-epithelia homeostasis in placentation, with implications in cancer dissemination.