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[PMID]:29236987
[Au] Autor:Kumar TR
[Ad] Endereço:Division of Reproductive Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
[Ti] Título:Extragonadal Actions of FSH: A Critical Need for Novel Genetic Models.
[So] Source:Endocrinology;159(1):2-8, 2018 01 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Follicle-stimulating hormone (FSH) is critical for ovarian folliculogenesis and essential for female fertility. FSH binds to FSH receptors (FSHRs) and regulates estrogen production in ovarian granulosa cells to orchestrate female reproductive physiology. Ovarian senescence that occurs as a function of aging results in loss of estrogen production, and this is believed to be the major reason for bone loss in postmenopausal women. Although conflicting, studies in rodents and humans during the last decade have provided genetic, pharmacological, and physiological evidence that elevated FSH levels that occur in the face of normal or declining estrogen levels directly regulate bone mass and adiposity. Recently, an efficacious blocking polyclonal FSHß antibody was developed that inhibited ovariectomy-induced bone loss and triggered white-to-brown fat conversion accompanied by mitochondrial biogenesis in mice. Moreover, additional nongonadal targets of FSH action have been identified, and these include the female reproductive tract (endometrium and myometrium), the placenta, hepatocytes, and blood vessels. In this mini-review, I summarize these studies in mice and humans and discuss critical gaps in our knowledge, yet unanswered questions, and the rationale for developing novel genetic models to unambiguously address the extragonadal actions of FSH.
[Mh] Termos MeSH primário: Envelhecimento
Hormônio Foliculoestimulante/fisiologia
Modelos Genéticos
Receptores do FSH/agonistas
Transdução de Sinais
[Mh] Termos MeSH secundário: Adiposidade
Animais
Desenvolvimento Ósseo
Feminino
Hormônio Foliculoestimulante/genética
Seres Humanos
Fígado/fisiologia
Masculino
Camundongos Knockout
Camundongos Transgênicos
Placentação
Gravidez
Receptores do FSH/genética
Receptores do FSH/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Receptors, FSH); 9002-68-0 (Follicle Stimulating Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03118


  2 / 2156 MEDLINE  
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[PMID]:29319820
[Au] Autor:Ashary N; Tiwari A; Modi D
[Ad] Endereço:Molecular and Cellular Biology Laboratory, National Institute for Research in Reproductive Health, Indian Council of Medical Research, Mumbai, India.
[Ti] Título:Embryo Implantation: War in Times of Love.
[So] Source:Endocrinology;159(2):1188-1198, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Contrary to widespread belief, the implantation of an embryo for the initiation of pregnancy is like a battle, in that the embryo uses a variety of coercive tactics to force its acceptance by the endometrium. We propose that embryo implantation involves a three-step process: (1) identification of a receptive endometrium; (2) superimposition of a blastocyst-derived signature onto the receptive endometrium before implantation; and finally (3) breaching by the embryo and trophoblast invasion, culminating in decidualization and placentation. We review here the story that is beginning to emerge, focusing primarily on the cells that are in "combat" during this process.
[Mh] Termos MeSH primário: Implantação do Embrião/fisiologia
Placentação/fisiologia
[Mh] Termos MeSH secundário: Animais
Blastocisto/fisiologia
Embrião de Mamíferos
Feminino
Seres Humanos
Gravidez
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03082


  3 / 2156 MEDLINE  
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[PMID]:29305264
[Au] Autor:Nikolaou S; Hadjikypri X; Ioannou G; Elia A; Georgiades P
[Ad] Endereço:Department of Biological Sciences, University of Cyprus, University Campus, P.O. Box 20537, 1678 Nicosia, Cyprus.
[Ti] Título:Functional and phenotypic distinction of the first two trophoblast subdivisions and identification of the border between them during early postimplantation: A prerequisite for understanding early patterning during placentogenesis.
[So] Source:Biochem Biophys Res Commun;496(1):64-69, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The early stages of mouse placentogenesis (placenta formation) involve poorly understood patterning events within polar trophectoderm-derived trophoblast, the progenitor of all placental trophoblast cell types. By early postimplantation [embryonic day 5.5 (E5.5)], this patterning causes early trophoblast to become subdivided into extraembryonic ectoderm (ExE) and ectoplacental cone (EPC). A prerequisite to understanding this patterning requires knowing the location of ExE-EPC border and being able to distinguish the entire ExE from EPC at E5.5/E6.5, a time when the proamnioitic cavity within ExE is not fully established. However, these issues are unknown, as they have not been directly addressed. Here, we directly addressed these using trophoblast explant culture to functionally test for the location of ExE-EPC border, combined with phenotypic characterization of trophoblast proximal and distal to it. We show for the first time that the proximal-distal level of ExE-EPC border within E5.5/E6.5 trophoblast coincides with where Reichert's membrane (outermost basement membrane of conceptus) inserts into early trophoblast and with the proximal limit of extraembryonic visceral endoderm (primitive endoderm derivative covering part of early trophoblast). Based on these novel findings, we discovered that (a) the entire E5.5/E6.5 ExE can be distinguished from EPC because it is epithelial and specifically expresses Erf and Claudin4 and (b) at E5.5/E6.5, the entire EPC differs from ExE in that it is not epithelial and specifically expresses Snail. This work is expected to contribute to understanding the cellular and molecular basis of early trophoblast patterning during placentogenesis.
[Mh] Termos MeSH primário: Padronização Corporal/fisiologia
Ectoderma/citologia
Desenvolvimento Embrionário/fisiologia
Endoderma/citologia
Placentação/fisiologia
Trofoblastos/citologia
Trofoblastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ectoderma/fisiologia
Endoderma/fisiologia
Feminino
Camundongos
Camundongos Endogâmicos ICR
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  4 / 2156 MEDLINE  
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[PMID]:28467908
[Au] Autor:Inoue K; Hirose M; Inoue H; Hatanaka Y; Honda A; Hasegawa A; Mochida K; Ogura A
[Ad] Endereço:Bioresource Engineering Division, BioResource Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan. Electronic address: inoue@rtc.riken.jp.
[Ti] Título:The Rodent-Specific MicroRNA Cluster within the Sfmbt2 Gene Is Imprinted and Essential for Placental Development.
[So] Source:Cell Rep;19(5):949-956, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) represent small noncoding RNAs that are involved in physiological and developmental processes by posttranscriptionally inhibiting gene expression. One of the largest miRNA clusters in mice is located in intron 10 of the Sfmbt2 gene, containing 72 miRNA precursor sequences. In this study, we generated mice lacking the entire Sfmbt2 miRNA cluster to elucidate its functions during development. The Sfmbt2 miRNAs were expressed predominantly from the paternal allele in the placenta, as is the host Sfmbt2 gene. Loss of the paternal allele resulted in severely impaired development of the placenta, especially the spongiotrophoblast layer, and frequent lethality or defects of fetuses. The predicted target sequences of the miRNAs and gene expression analysis defined at least nine putative target genes, which function as tumor suppressors or apoptosis inducers. Our study has provided experimental evidence for the indispensable roles of placental miRNAs in trophoblast proliferation and thus fetal development.
[Mh] Termos MeSH primário: Impressão Genômica
MicroRNAs/genética
Placentação/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
MicroRNAs/metabolismo
Placenta/metabolismo
Gravidez
Fatores de Transcrição/metabolismo
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Sfmbt2 protein, mouse); 0 (Transcription Factors); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  5 / 2156 MEDLINE  
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[PMID]:29203625
[Au] Autor:Kaartokallio T; Utge S; Klemetti MM; Paananen J; Pulkki K; Romppanen J; Tikkanen I; Heinonen S; Kajantie E; Kere J; Kivinen K; Pouta A; Lakkisto P; Laivuori H
[Ad] Endereço:From Medical and Clinical Genetics, Helsinki University Hospital (T.K., S.U., M.M.K., H.L.), Obstetrics and Gynaecology, Helsinki University Hospital (M.M.K., S.H.), Abdominal Center, Nephrology, Helsinki University Hospital (I.T.), Clinical Chemistry and Hematology, Helsinki University Hospital (P.
[Ti] Título:Fetal Microsatellite in the Heme Oxygenase 1 Promoter Is Associated With Severe and Early-Onset Preeclampsia.
[So] Source:Hypertension;71(1):95-102, 2018 01.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preeclampsia is a vascular pregnancy disorder that often involves impaired placental development. HO-1 (heme oxygenase 1, encoded by ) is a stress response enzyme crucial for endothelial and placental function. Long version of the guanine-thymine (GT ) microsatellite in the promoter decreases HO-1 expression, and the long maternal repeat is associated with late-onset preeclampsia. Our aim was to study whether the length of fetal repeat is associated with mother's preeclampsia, whether the length of fetal and maternal repeats affect HO-1 levels in placenta and maternal serum, and whether HO-1 levels are altered in preeclampsia. We genotyped the repeat in the cord blood of 609 preeclamptic and 745 nonpreeclamptic neonates. HO-1 levels were measured in 36 placental samples, and in the first (222 cases/243 controls) and third (176 cases/53 controls) pregnancy trimester serum samples using enzyme-linked immunosorbent assay. The long fetal GT repeat was associated with preeclampsia and its severe and early-onset subtypes. Interaction analysis suggested the maternal and fetal effects to be independent. Placental or serum HO-1 levels were not altered in preeclamptics, possibly reflecting heterogeneity of preeclampsia. Carriers of the long fetal and maternal repeats had lower placental and serum HO-1 levels, respectively, providing functional evidence for the association. We conclude that the long fetal GT repeat may increase mother's risk for especially severe and early-onset preeclampsia. The fetal and maternal risk alleles likely predispose to different disease subtypes.
[Mh] Termos MeSH primário: Feto/fisiologia
Heme Oxigenase-1/genética
Repetições de Microssatélites/genética
Placentação/genética
Pré-Eclâmpsia
[Mh] Termos MeSH secundário: Adulto
Feminino
Predisposição Genética para Doença
Heme Oxigenase-1/metabolismo
Seres Humanos
Pré-Eclâmpsia/diagnóstico
Pré-Eclâmpsia/genética
Pré-Eclâmpsia/fisiopatologia
Gravidez
Regiões Promotoras Genéticas/fisiologia
Índice de Gravidade de Doença
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.10425


  6 / 2156 MEDLINE  
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[PMID]:29259074
[Au] Autor:Chang CW; Wakeland AK; Parast MM
[Ad] Endereço:Department of PathologyUniversity of California San Diego, La Jolla, California, USA.
[Ti] Título:Trophoblast lineage specification, differentiation and their regulation by oxygen tension.
[So] Source:J Endocrinol;236(1):R43-R56, 2018 Jan.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Development of the early embryo takes place under low oxygen tension. Under such conditions, the embryo implants and the trophectoderm, the outer layer of blastocyst, proliferate, forming the cytotrophoblastic shell, the early placenta. The cytotrophoblasts (CTBs) are the so-called epithelial 'stem cells' of the placenta, which, depending on the signals they receive, can differentiate into either extravillous trophoblast (EVT) or syncytiotrophoblast (STB). EVTs anchor the placenta to the uterine wall and remodel maternal spiral arterioles in order to provide ample blood supply to the growing fetus. STBs arise through CTB fusion, secrete hormones necessary for pregnancy maintenance and form a barrier across which nutrient and gas exchange can take place. The bulk of EVT differentiation occurs during the first trimester, before the onset of maternal arterial blood flow into the intervillous space of the placenta, and thus under low oxygen tension. These conditions affect numerous signaling pathways, including those acting through hypoxia-inducible factor, the nutrient sensor mTOR and the endoplasmic reticulum stress-induced unfolded protein response pathway. These pathways are known to be involved in placental development and disease, and specific components have even been identified as directly involved in lineage-specific trophoblast differentiation. Nevertheless, much controversy surrounds the role of hypoxia in trophoblast differentiation, particularly with EVT. This review summarizes previous studies on this topic, with the intent of integrating these results and synthesizing conclusions that resolve some of the controversy, but then also pointing to remaining areas, which require further investigation.
[Mh] Termos MeSH primário: Diferenciação Celular
Oxigênio/fisiologia
Placentação
Trofoblastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Feminino
Seres Humanos
Hipóxia/fisiopatologia
Doenças Placentárias/etiologia
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0402


  7 / 2156 MEDLINE  
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[PMID]:28081642
[Au] Autor:Ballering G; Leijnse J; Eijkelkamp N; Peeters L; de Heus R
[Ad] Endereço:a Department of Obstetrics , University Medical Centre Utrecht , Utrecht , the Netherlands.
[Ti] Título:First-trimester placental vascular development in multiparous women differs from that in nulliparous women.
[So] Source:J Matern Fetal Neonatal Med;31(2):209-215, 2018 Jan.
[Is] ISSN:1476-4954
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Multiparas differ from nulliparas by delivering larger babies with larger placentas and by having a lower risk of developing placental syndromes. We postulate that these differences result from a different initial course of placental vascular development. STUDY DESIGN: We measured placental flow index (FI), vascularization index (VI) and placental volume by 3D power Doppler and obtained blood samples at 8, 10 and 12 weeks pregnancy in 34 healthy nulliparous and 16 multiparous women with an uneventful pregnancy. RESULTS: Between 8 and 12 weeks multiparas differed from nulliparas in a more rapid initial rise in FI, a higher angiopoietin-2 (ang2) level at eight weeks and no decline in the VEGF/sVEGF-R ratio. Nevertheless, at 12 weeks the FI and placental volume were indistinguishable between both study groups. CONCLUSIONS: These results combining serially measured placental vascularization, placental volume and circulating angiogenetic factors show initial differences in placental development, that howeve, did not maintain till the end of first trimester. The results support the concept that early placental vascular development differs between nulliparas and multiparas. Nevertheless, it is unclear whether these differences contribute to the development later on in pregnancy of intergroup differences in birthweight and incidence of placental syndromes.
[Mh] Termos MeSH primário: Paridade/fisiologia
Placenta/irrigação sanguínea
Placentação/fisiologia
Primeiro Trimestre da Gravidez/fisiologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Imagem Tridimensional
Placenta/diagnóstico por imagem
Gravidez
Primeiro Trimestre da Gravidez/sangue
Estudos Prospectivos
Ultrassonografia Doppler
Ultrassonografia Pré-Natal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1080/14767058.2017.1280020


  8 / 2156 MEDLINE  
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[PMID]:28751574
[Au] Autor:Xiao J; Feng Y; Li X; Li W; Fan L; Liu J; Zeng X; Chen K; Chen X; Zhou X; Zheng XL; Chen S
[Ad] Endereço:From the Department of Obstetrics & Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China (J.X., Y.F., W.L., L.F., J.L., X. Zeng, K.C., X.C., S.C.); Department of Urology, Zhengzhou First People's Hospital, Henan, China (X.L.); De
[Ti] Título:Expression of ADAMTS13 in Normal and Abnormal Placentae and Its Potential Role in Angiogenesis and Placenta Development.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1748-1756, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 repeats, member 13) is primarily synthesized in liver. The biosynthesis of ADAMTS13 and its physiological role in placenta are not known. APPROACH AND RESULTS: We used real-time polymerase chain reaction, immunohistochemistry, and Western blotting analyses, as well as proteolytic cleavage of FRETS (fluorescent resonance energy transfers)-VWF73, to determine ADAMTS13 expression in placenta and trophoblasts obtained from individuals with normal pregnancy and patients with severe preeclampsia. We also determined the role of ADAMTS13 in extravillous trophoblasts using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound scratch assay, transwell migration assay, tube formation assay, and tissue outgrowth assays. We showed that full-length and proteolytically active ADAMTS13 was expressed in normal human placenta, primarily in the trophoblasts and villous core fetal vessel endothelium during pregnancy. Placental expression of mRNA, protein, and proteolytic activity was at the highest levels during the first trimester and significantly reduced at the term of gestation. Additionally, significantly reduced levels of placental ADAMTS13 expression was detected under hypoxic conditions and in patients with preeclampsia. In addition, recombinant ADAMTS13 protease stimulated proliferation, migration, invasion, and network formation of trophoblastic cells in culture. Finally, knockdown of ADAMTS13 expression attenuated the ability of tube formation in trophoblast (HTR-8/SVNEO) cells and the extravillous trophoblast outgrowth in placental explants. CONCLUSIONS: Our results demonstrate for the first time the expression of mRNA and protein in normal and abnormal placental tissues and its role in promoting angiogenesis and trophoblastic cell development. The findings support the potential role of the ADAMTS13-von Willebrand factor pathway in normal pregnancy and pathogenesis of preeclampsia.
[Mh] Termos MeSH primário: Proteína ADAMTS13/metabolismo
Células Endoteliais/enzimologia
Neovascularização Fisiológica
Placenta/irrigação sanguínea
Placenta/enzimologia
Placentação
Pré-Eclâmpsia/enzimologia
[Mh] Termos MeSH secundário: Proteína ADAMTS13/genética
Adulto
Animais
Células CHO
Estudos de Casos e Controles
Movimento Celular
Proliferação Celular
Cricetulus
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Pré-Eclâmpsia/genética
Pré-Eclâmpsia/fisiopatologia
Gravidez
Trimestres da Gravidez
Proteólise
Interferência de RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Técnicas de Cultura de Tecidos
Transfecção
Trofoblastos/enzimologia
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (von Willebrand Factor); EC 3.4.24.87 (ADAMTS13 Protein); EC 3.4.24.87 (ADAMTS13 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309735


  9 / 2156 MEDLINE  
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[PMID]:28727763
[Au] Autor:Kadmiel M; Matson BC; Espenschied ST; Lenhart PM; Caron KM
[Ad] Endereço:Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.
[Ti] Título:Loss of receptor activity-modifying protein 2 in mice causes placental dysfunction and alters PTH1R regulation.
[So] Source:PLoS One;12(7):e0181597, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Receptor activity-modifying protein 2 (Ramp2) is a single-pass transmembrane protein that heterodimerizes with several family B G-protein coupled receptors to alter their function. Ramp2 has been primarily characterized in association with calcitonin receptor-like receptor (Calcrl, CLR), forming the canonical receptor complex for the endocrine peptide adrenomedullin (Adm, AM). However, we previously demonstrated that Ramp2+/- female mice display a constellation of endocrine-related phenotypes that are distinct from those of Adm+/- and Calcrl+/- mice, implying that RAMP2 has physiological functions beyond its canonical complex. Here, we localize Ramp2 expression in the mouse placenta, finding that Ramp2 is robustly expressed in the fetal labyrinth layer, and then characterize the effects of loss of Ramp2 on placental development. Consistent with the expression pattern of Ramp2 in the placenta, Ramp2-/- placentas have a thinner labyrinth layer with significantly fewer trophoblast cells secondary to a reduction in trophoblast proliferation. We also find that absence of Ramp2 leads to failed spiral artery remodeling unaccompanied by changes in the uterine natural killer cell population. Furthermore, we assess changes in gene expression of other RAMP2-associated G-protein coupled receptors (GPCRs), concluding that Ramp2 loss decreases parathyroid hormone 1 receptor (Pthr1) expression and causes a blunted response to systemic parathyroid hormone (PTH) administration in mice. Ultimately, these studies provide in vivo evidence of a role for RAMP2 in placental development distinct from the RAMP2-CLR/AM signaling paradigm and identify additional pathways underlying the endocrine and fertility defects of the previously characterized Ramp2 heterozygous adult females.
[Mh] Termos MeSH primário: Doenças Placentárias/metabolismo
Placenta/metabolismo
Placentação/fisiologia
Proteína 2 Modificadora da Atividade de Receptores/deficiência
Receptor Tipo 1 de Hormônio Paratireóideo/metabolismo
[Mh] Termos MeSH secundário: Adrenomedulina/metabolismo
Animais
Proteína Semelhante a Receptor de Calcitonina/metabolismo
Proliferação Celular/fisiologia
Feminino
Expressão Gênica
Haploinsuficiência/fisiologia
Camundongos da Linhagem 129
Camundongos Knockout
Modelos Animais
Hormônio Paratireóideo/metabolismo
Placenta/irrigação sanguínea
Placenta/patologia
Doenças Placentárias/patologia
Gravidez
RNA Mensageiro/metabolismo
Proteína 2 Modificadora da Atividade de Receptores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcitonin Receptor-Like Protein); 0 (PTH1R protein, mouse); 0 (Parathyroid Hormone); 0 (RNA, Messenger); 0 (Ramp2 protein, mouse); 0 (Receptor Activity-Modifying Protein 2); 0 (Receptor, Parathyroid Hormone, Type 1); 148498-78-6 (Adrenomedullin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181597


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[PMID]:28683173
[Au] Autor:Simic M; Wikström AK; Stephansson O
[Ad] Endereço:Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska University Hospital and Institutet, Stockholm, Sweden.
[Ti] Título:Accelerated fetal growth in early pregnancy and risk of severe large-for-gestational-age and macrosomic infant: a cohort study in a low-risk population.
[So] Source:Acta Obstet Gynecol Scand;96(10):1261-1268, 2017 Oct.
[Is] ISSN:1600-0412
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Our objective was to examine the association between fetal growth in early pregnancy and risk of severe large-for-gestational-age (LGA) and macrosomia at birth in a low-risk population. MATERIAL AND METHODS: Cohort study that included 68 771 women with non-anomalous singleton pregnancies, without history of diabetes or hypertension, based on an electronic database on pregnancies and deliveries in Stockholm-Gotland Region, Sweden, 2008-2014. We performed multivariable logistic regression to estimate the association between accelerated fetal growth occurring in the first through early second trimester as measured by ultrasound and LGA and macrosomia at birth. Restricted analyses were performed in the groups without gestational diabetes and with normal body mass index (18.5-24.9 kg/m ). RESULTS: When adjusting for confounders, the odds of having a severely LGA or macrosomic infant were elevated in mothers with fetuses that were at least 7 days larger than expected as compared with mothers without age discrepancy at the second-trimester scan (adjusted odds ratio 1.80; 95% CI 1.23-2.64 and adjusted odds ratio 2.15; 95% CI 1.55-2.98, respectively). Additionally, mothers without gestational diabetes and mothers with normal weight had an elevated risk of having a severely LGA or macrosomic infant when the age discrepancy by second-trimester ultrasound was at least 7 days. CONCLUSIONS: In a low-risk population, ultrasound-estimated accelerated fetal growth in early pregnancy was associated with an increased risk of having a severely LGA or macrosomic infant.
[Mh] Termos MeSH primário: Desenvolvimento Fetal/fisiologia
Macrossomia Fetal
Peso Fetal
Primeiro Trimestre da Gravidez
[Mh] Termos MeSH secundário: Peso Corporal
Estudos de Coortes
Feminino
Seres Humanos
Recém-Nascido
Placentação
Gravidez
Segundo Trimestre da Gravidez
Medição de Risco
Suécia
Ultrassonografia Pré-Natal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1111/aogs.13189



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