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[PMID]:28433367
[Au] Autor:Wang ET; Kathiresan ASQ; Bresee C; Greene N; Alexander C; Pisarska MD
[Ad] Endereço:Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California.
[Ti] Título:Abnormal implantation after fresh and frozen in vitro fertilization cycles.
[So] Source:Fertil Steril;107(5):1153-1158, 2017 May.
[Is] ISSN:1556-5653
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine whether fresh embryo transfers are at a higher risk of abnormal implantation compared with frozen embryo transfers while accounting for the embryo stage at transfer. DESIGN: Retrospective cohort study. SETTING: Not applicable. PATIENT(S): We used data from the Society for Assisted Reproductive Technologies to identify all fresh and frozen autologous IVF cycles from 2004-2013 resulting in a positive pregnancy test. The cycles were parameterized into a four-level predictor of [1] fresh blastocyst transfer, [2] fresh non-blastocyst transfer, [3] frozen blastocyst transfer, and [4] frozen non-blastocyst transfer. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): We examined a composite outcome of abnormal implantation, defined as biochemical pregnancy, ectopic/heterotopic pregnancy, and first-trimester pregnancy loss. Regression modeling was performed with repeated measures multivariable logistic regression, adjusted for age, parity, number of embryos transferred, infertility diagnosis, and calendar year of treatment. RESULT(S): Of 509,938 cycles analyzed, 31.8% resulted in abnormal implantation. Compared with a fresh blastocyst transfer, a fresh non-blastocyst transfer had a 22% increase risk of abnormal implantation, a frozen blastocyst transfer had a 36% increase risk, and a frozen non-blastocyst transfer had a 57% increase risk. When individual outcomes were analyzed, fresh embryo transfers had a lower risk of biochemical pregnancy and pregnancy loss but a higher risk for ectopic/heterotopic pregnancy. CONCLUSION(S): Fresh blastocyst transfers had the lowest overall risk of abnormal implantation but a higher risk of ectopic/heterotopic pregnancy. Although embryo cryopreservation is indicated in certain treatment cycles, elective embryo cryopreservation may not be the optimal strategy to adopt for all cycles.
[Mh] Termos MeSH primário: Criopreservação/utilização
Perda do Embrião/mortalidade
Transferência Embrionária/mortalidade
Infertilidade/mortalidade
Infertilidade/terapia
Resultado da Gravidez/epidemiologia
Gravidez Ectópica/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Adulto
Distribuição por Idade
Estudos de Coortes
Criopreservação/métodos
Transferência Embrionária/utilização
Feminino
Fertilização In Vitro
Seres Humanos
Incidência
Meia-Idade
Gravidez
Estudos Retrospectivos
Fatores de Risco
Estados Unidos/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170424
[St] Status:MEDLINE


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[PMID]:28368537
[Au] Autor:Cheng J; Rosario G; Cohen TV; Hu J; Stewart CL
[Ad] Endereço:Cancer and Developmental Biology Laboratory, Division of Basic Science, National Cancer Institute at Frederick, Frederick, Maryland 21702.
[Ti] Título:Tissue-Specific Ablation of the LIF Receptor in the Murine Uterine Epithelium Results in Implantation Failure.
[So] Source:Endocrinology;158(6):1916-1928, 2017 Jun 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokine leukemia inhibitory factor (LIF) is essential for rendering the uterus receptive for blastocyst implantation. In mice, LIF receptor expression (LIFR) is largely restricted to the uterine luminal epithelium (LE). LIF, secreted from the endometrial glands (GEs), binds to the LIFR, activating the Janus kinase-signal transducer and activation of transcription (STAT) 3 (Jak-Stat3) signaling pathway in the LE. JAK-STAT activation converts the LE to a receptive state so that juxtaposed blastocysts begin to implant. To specifically delete the LIFR in the LE, we derived a line of mice in which Cre recombinase was inserted into the endogenous lactoferrin gene (Ltf-Cre). Lactoferrin expression in the LE is induced by E2, and we demonstrate that Cre recombinase activity is restricted to the LE and GE. To determine the requirement of the LIFR in implantation, we derived an additional mouse line carrying a conditional (floxed) Lifrflx/flx gene. Crossing Ltf-Cre mice with Lifrflx/flx mice generated Lifrflx/Δ:LtfCre/+ females that were overtly normal but infertile. Many of these females, despite repeated matings, did not become pregnant. Unimplanted blastocysts were recovered from the Lifrflx/Δ:LtfCre/+ uteri and, when transferred to wild-type recipients, implanted normally, indicating that uterine receptivity rather than the embryo's competency is compromised. The loss of Lifr results in both the failure for STAT3 to translocate to the LE nuclei and a reduction in the expression of the LIF regulated gene Msx1 that regulates uterine receptivity. These results reveal that uterine expression of the LIFR is essential for embryo implantation and further define the components of the LIF signaling pathway necessary for effective implantation.
[Mh] Termos MeSH primário: Implantação do Embrião/genética
Perda do Embrião/genética
Subunidade alfa de Receptor de Fator Inibidor de Leucemia/genética
Útero/metabolismo
[Mh] Termos MeSH secundário: Animais
Perda do Embrião/metabolismo
Perda do Embrião/patologia
Embrião de Mamíferos
Epitélio/metabolismo
Feminino
Subunidade alfa de Receptor de Fator Inibidor de Leucemia/metabolismo
Camundongos
Camundongos Knockout
Especificidade de Órgãos/genética
Gravidez
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leukemia Inhibitory Factor Receptor alpha Subunit); 0 (Lifr protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00103


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[PMID]:28320871
[Au] Autor:Ohgaki R; Ohmori T; Hara S; Nakagomi S; Kanai-Azuma M; Kaneda-Nakashima K; Okuda S; Nagamori S; Kanai Y
[Ad] Endereço:Department of Bio-system Pharmacology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
[Ti] Título:Essential Roles of L-Type Amino Acid Transporter 1 in Syncytiotrophoblast Development by Presenting Fusogenic 4F2hc.
[So] Source:Mol Cell Biol;37(11), 2017 Jun 01.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The layers of the epithelial syncytium, i.e., syncytiotrophoblasts, differentiate from chorionic trophoblasts via cell fusion and separate maternal and fetal circulations in hemochorial placentas. L-type amino acid transporter 1 (LAT1) and its covalently linked ancillary subunit 4F2hc are colocalized on both maternal and fetal surfaces of syncytiotrophoblasts, implying their roles in amino acid transfer through the placental barrier. In this study, LAT1 knockout, in addition, revealed a novel role of LAT1 in syncytiotrophoblast development. LAT1 at midgestation was selectively expressed in trophoblastic lineages in the placenta, exclusively as a LAT1-4F2hc heterodimer. In LAT1 homozygous knockout mice, chorionic trophoblasts remained largely mononucleated, and the layers of syncytiotrophoblasts were almost completely absent. The amount of 4F2hc protein, which possesses a fusogenic function in trophoblastic cells, as well as in virus-infected cells, was drastically reduced by LAT1 knockout, with less affecting the mRNA level. Knockdown of LAT1 in trophoblastic BeWo cells also reduced 4F2hc protein and suppressed forskolin-induced cell fusion. These results demonstrate a novel fundamental role of LAT1 to support the protein expression of 4F2hc via a chaperone-like function in chorionic trophoblasts and to promote syncytiotrophoblast formation by contributing to cell fusion in the developing placenta.
[Mh] Termos MeSH primário: Cadeia Pesada da Proteína-1 Reguladora de Fusão/metabolismo
Transportador 1 de Aminoácidos Neutros Grandes/metabolismo
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Fusão Celular
Linhagem Celular
Linhagem da Célula
Proliferação Celular/efeitos dos fármacos
Colforsina/farmacologia
Cruzamentos Genéticos
Perda do Embrião/patologia
Feminino
Deleção de Genes
Técnicas de Silenciamento de Genes
Marcação de Genes
Homozigoto
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Placenta/anormalidades
Placenta/efeitos dos fármacos
Gravidez
Trofoblastos/citologia
Trofoblastos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fusion Regulatory Protein 1, Heavy Chain); 0 (Large Neutral Amino Acid-Transporter 1); 1F7A44V6OU (Colforsin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28249007
[Au] Autor:Moraes-Souza RQ; Reinaque AP; Soares TS; Silva AL; Giunchetti RC; Takano MA; Akamatsu MA; Kubrusly FS; Lúcio-Macarini F; Raw I; Iourtov D; Ho PL; Bueno LL; Fujiwara RT; Volpato GT
[Ad] Endereço:Laboratory of System Physiology and Reproductive Toxicology, Institute of Biological and Health Sciences, Federal University of Mato Grosso (UFMT) - Barra do Garças, Mato Grosso State, Brazil.
[Ti] Título:Safety evaluation of a vaccine: Effect in maternal reproductive outcome and fetal anomaly frequency in rats using a leishmanial vaccine as a model.
[So] Source:PLoS One;12(3):e0172525, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While the immunogenic potential of the vaccination against infectious diseases was extensively shown, data on the safety assessment of recombinant proteins in vaccine formulations administered during pregnancy are still scarce. In the current study, the antigenicity of a vaccine against leishmaniasis (based on Leishmania braziliensis recombinant protein peroxidoxin) during pregnancy and possible maternal reproductive outcomes and fetal anomalies after immunization with a leishmanial vaccine or adjuvant alone (Bordetella pertussis derived MPLA adjuvant) were assessed. Rats were mated and allocated in three groups: Control-rats received saline; Adjuvant-rats received the adjuvant MPLA, and Vaccine-rats received the combination of MPLA and peroxidoxin. The administration was subcutaneously at the dorsal region, three times (days 0, 7, 14 of pregnancy). On day 21 of pregnancy, all rats were bled for biochemical and immunological measurements. The gravid uterus was weighed with its contents, and the fetuses were analyzed. The immunization with peroxidoxin induced a significant production of circulating IgG levels compared to other groups but caused a significant in post-implantation loss (14.7%) when compared to Control (5.0%) and Adjuvant (4.4%) groups. Furthermore, a significantly high rate of fetal visceral anomalies, such as hydronephrosis and convoluted ureter, was also observed in animals that received vaccine when compared to Control or Adjuvant groups. These data indicate the importance of safety evaluation of vaccines during pregnancy and the limited use of peroxidoxin administration during pregnancy. More importantly, the safety monitoring of immunization with MPLA derived from Bordetella pertussis demonstrated no reproductive outcomes associated with adjuvant administration, suggesting its safe use during pregnancy.
[Mh] Termos MeSH primário: Perda do Embrião/induzido quimicamente
Feto/anormalidades
Leishmania braziliensis
Vacinas contra Leishmaniose/efeitos adversos
Exposição Materna/efeitos adversos
Modelos Biológicos
Peroxirredoxinas/efeitos adversos
Proteínas de Protozoários/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Anticorpos Antiprotozoários/imunologia
Avaliação Pré-Clínica de Medicamentos
Feminino
Feto/imunologia
Imunoglobulina G/imunologia
Vacinas contra Leishmaniose/imunologia
Vacinas contra Leishmaniose/farmacologia
Peroxirredoxinas/imunologia
Peroxirredoxinas/farmacologia
Gravidez
Proteínas de Protozoários/imunologia
Proteínas de Protozoários/farmacologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Protozoan); 0 (Immunoglobulin G); 0 (Leishmaniasis Vaccines); 0 (Protozoan Proteins); EC 1.11.1.15 (Peroxiredoxins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172525


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[PMID]:28153493
[Au] Autor:Koyama S; Fukuda K; Watanabe S; Matsushita A; Tsuchiya H; Fujinami N; Kohara S; Murayama N; Nagano M; Yamazaki H; Fukuzaki K; Uno Y; Hosoi Y
[Ad] Endereço:Drug Safety Research Center (DSR), Shin Nippon Biomedical Laboratories (SNBL), Ltd., Kagoshima, Japan; SNBL USA, Ltd., Everett, WA, USA.
[Ti] Título:CYP2C76 deficiency is embryonic lethal in cynomolgus macaques: The potential role of CYP2C76 in early embryogenesis.
[So] Source:Drug Metab Pharmacokinet;32(1):112-115, 2017 Feb.
[Is] ISSN:1880-0920
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cynomolgus macaques are an important primate species for drug metabolism studies; however cynomolgus CYP2C76, an important drug-metabolizing enzyme, accounts for drug metabolism differences to humans, so that CYP2C76-null animals might show drug-metabolizing properties more similar to humans. In this study, attempts were made to produce CYP2C76-null animals by assisted reproduction technology. Oocytes and sperm collected from the heterozygotes for the null allele (c.449TG > A) were subjected to intracytoplasmic sperm injection, and the embryos produced were cultured in vitro through the blastocyst stage. Preimplantation genetic diagnosis using a biopsied portion of the blastocyst revealed that none of the 32 blastocysts analyzed were homozygotes. In contrast, 2 of the 20 embryos analyzed were homozygotes at the 8-cell stage, indicating that CYP2C76-null embryos most likely stop developing between the 8-cell and blastocyst stage. By polymerase chain reaction, expression of CYP2C76 mRNA was detected in oocytes and blastocysts, but not in 2-, 4-, 8-, or 16/32-cell stage embryos. Metabolic assays showed that CYP2C76 metabolized progesterone. These results indicated that CYP2C76 null was likely embryonic lethal, suggesting its potential role during early embryogenesis in cynomolgus macaques.
[Mh] Termos MeSH primário: Sistema Enzimático do Citocromo P-450/deficiência
Sistema Enzimático do Citocromo P-450/metabolismo
Perda do Embrião/genética
Desenvolvimento Embrionário
Macaca fascicularis/embriologia
Macaca fascicularis/genética
[Mh] Termos MeSH secundário: Animais
Sistema Enzimático do Citocromo P-450/genética
Feminino
Masculino
Oócitos/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Espermatozoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (cytochrome P-450 CYP2C subfamily); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE


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[PMID]:28099717
[Au] Autor:Ibrahim MI; Ramy AR; Abdelhamid AS; Ellaithy MI; Omar A; Harara RM; Fathy H; Abolouz AS
[Ad] Endereço:Department of Obstetrics and Gynecology, Ain Shams University Faculty of Medicine, Cairo, Egypt.
[Ti] Título:Maternal serum amyloid A level as a novel marker of primary unexplained recurrent early pregnancy loss.
[So] Source:Int J Gynaecol Obstet;136(3):298-303, 2017 Mar.
[Is] ISSN:1879-3479
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess maternal serum amyloid A (SAA) levels among women with primary unexplained recurrent early pregnancy loss (REPL). METHODS: A prospective study was conducted among women with missed spontaneous abortion in the first trimester at Ain Shams University Maternity Hospital, Cairo, Egypt, between January 21 and December 25, 2014. Women with at least two consecutive primary unexplained REPLs and no previous live births were enrolled. A control group was formed of women with no history of REPL who had at least one previous uneventful pregnancy with no adverse outcomes. Serum samples were collected to measure SAA levels. The main outcome was the association between SAA and primary unexplained REPL. RESULTS: Each group contained 96 participants. Median SAA level was significantly higher among women with REPL (50.0 µg/mL, interquartile range 26.0-69.0) than among women in the control group (11.6 µg/mL, interquartile range 6.2-15.5; P<0.001). The SAA level was an independent indicator of primary unexplained REPL, after adjusting for maternal age and gestational age (odds ratio 1.12, 95% confidence interval 1.06-1.19; P<0.001). CONCLUSION: Elevated SAA levels found among women with primary unexplained REPL could represent a novel biomarker for this complication of pregnancy.
[Mh] Termos MeSH primário: Aborto Habitual/sangue
Perda do Embrião/sangue
Primeiro Trimestre da Gravidez/sangue
Proteína Amiloide A Sérica/análise
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Egito
Feminino
Seres Humanos
Modelos Logísticos
Idade Materna
Análise Multivariada
Gravidez
Estudos Prospectivos
Curva ROC
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Serum Amyloid A Protein)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1002/ijgo.12076


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[PMID]:28079294
[Au] Autor:Suto JI
[Ad] Endereço:Animal Bioregulation Unit, Institute of Agrobiological Sciences, Division of Animal Sciences, National Agriculture and Food Research Organization (NARO), Tsukuba, Japan.
[Ti] Título:Locus on chromosome 16 is significantly associated with increased tendency to lose pups in females of the RR/Sgn inbred mouse strain.
[So] Source:Congenit Anom (Kyoto);57(2):57-60, 2017 Mar.
[Is] ISSN:1741-4520
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Females of the inbred mouse strain RR/Sgn have an apparent tendency to lose pups during rearing. To identify genes underlying this abnormal maternal phenotype, we performed quantitative trait loci (QTL) mapping in 349 (C57BL/6 J × RR/Sgn) F  × RR/Sgn backcross mice and identified one significant and one suggestive QTL on chromosomes 16 and 4, respectively. We assigned the gene symbol nurturing ability QTL 3 (Naq3) to the QTL on chromosome 16. Twenty of the 21 mothers who lost entire litters were homozygous for RR/Sgn allele at Naq3; i.e., the significant association of Naq3 with pup loss was further confirmed by binomial tests. We tentatively propose that Mapk1, Kalrn, and Vps8 are potential candidate genes for Naq3.
[Mh] Termos MeSH primário: Aborto Espontâneo/genética
Cromossomos Humanos Par 16/genética
Perda do Embrião/genética
Locos de Características Quantitativas
[Mh] Termos MeSH secundário: Alelos
Animais
Mapeamento Cromossômico
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos
Mães
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.1111/cga.12199


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[PMID]:28005395
[Au] Autor:Clark NC; Pru CA; Yee SP; Lydon JP; Peluso JJ; Pru JK
[Ad] Endereço:Department of Animal Sciences, Center for Reproductive Biology, Washington State University, Pullman, Washington.
[Ti] Título:Conditional Ablation of Progesterone Receptor Membrane Component 2 Causes Female Premature Reproductive Senescence.
[So] Source:Endocrinology;158(3):640-651, 2017 03 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nonclassical progesterone receptors progesterone receptor membrane component (PGRMC) 1 and PGRMC2 have been implicated in regulating cell survival of endometrial and ovarian cells in vitro and are abundantly expressed in these cell types. The objective of this study was to determine if Pgrmc1 and Pgrmc2 are essential for normal female reproduction. To accomplish this objective, Pgrmc1 and/or Pgrmc2 floxed mice (Pgrmc2fl/fl and Pgrmc1/2fl/fl) were crossed with Pgr-cre mice, which resulted in the conditional ablation of Pgrmc1 and/or Pgrmc2 from female reproductive tissues (i.e.,Pgrmc2d/d and Pgrmc1/2d/d mice). A breeding trial revealed that conditional ablation of Pgrmc2 initially led to subfertility, with Pgrmc2d/d female mice producing 47% fewer pups/litter than Pgrmc2fl/fl mice (P = 0.001). Pgrmc2d/d mice subsequently underwent premature reproductive senescence by parities 2 to 5, producing 37.8% fewer litters overall during the trial compared with Pgrmc2fl/fl mice (P = 0.020). Similar results were observed with Pgrmc1/2d/d mice. Based on ovarian morphology and serum P4, the subfertility/infertility was not due to faulty ovulation or luteal insufficiency. Rather an analysis of midgestation implantation sites revealed that postimplantation embryonic death was the major cause of the subfertility/infertility. As with our previous report of Pgrmc1d/d mice, Pgrmc2d/d and Pgrmc1/2d/d mice developed endometrial cysts consistent with accelerated aging of this tissue. Given the timing of postimplantation embryonic demise, uterine decidualization may be disrupted in mice deficient in PGRMC2 or PGRMC1/2. Overall, this study revealed that Pgrmc1 and/or Pgrmc2 are required for the maintenance of uterine histoarchitecture and normal female reproductive lifespan.
[Mh] Termos MeSH primário: Fertilidade
Proteínas de Membrana/fisiologia
Ovário/fisiologia
Receptores de Progesterona/fisiologia
Útero/fisiologia
[Mh] Termos MeSH secundário: Senilidade Prematura/genética
Senilidade Prematura/patologia
Animais
Perda do Embrião
Feminino
Camundongos
Camundongos Transgênicos
Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (PGRMC1 protein, mouse); 0 (PGRMC2 protein, mouse); 0 (Receptors, Progesterone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1701


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[PMID]:27994054
[Au] Autor:Xiao Y; Ma H; Wan P; Qin D; Wang X; Zhang X; Xiang Y; Liu W; Chen J; Yi Z; Li L
[Ad] Endereço:From the State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, 100101 Beijing.
[Ti] Título:Trp-Asp (WD) Repeat Domain 1 Is Essential for Mouse Peri-implantation Development and Regulates Cofilin Phosphorylation.
[So] Source:J Biol Chem;292(4):1438-1448, 2017 Jan 27.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trp-Asp (WD) repeat domain 1 (WDR1) is a highly conserved actin-binding protein across all eukaryotes and is involved in numerous actin-based processes by accelerating Cofilin severing actin filament. However, the function and the mechanism of WDR1 in mammalian early development are still largely unclear. We now report that WDR1 is essential for mouse peri-implantation development and regulates Cofilin phosphorylation in mouse cells. The disruption of maternal WDR1 does not obviously affect ovulation and female fertility. However, depletion of zygotic WDR1 results in embryonic lethality at the peri-implantation stage. In WDR1 knock-out cells, we found that WDR1 regulates Cofilin phosphorylation. Interestingly, WDR1 is overdosed to regulate Cofilin phosphorylation in mouse cells. Furthermore, we showed that WDR1 interacts with Lim domain kinase 1 (LIMK1), a well known phosphorylation kinase of Cofilin. Altogether, our results provide new insights into the role and mechanism of WDR1 in physiological conditions.
[Mh] Termos MeSH primário: Fatores de Despolimerização de Actina/metabolismo
Implantação do Embrião
Embrião de Mamíferos/embriologia
Desenvolvimento Embrionário
Quinases Lim/metabolismo
Proteínas dos Microfilamentos/metabolismo
[Mh] Termos MeSH secundário: Fatores de Despolimerização de Actina/genética
Animais
Perda do Embrião/genética
Perda do Embrião/metabolismo
Feminino
Quinases Lim/genética
Camundongos
Camundongos Knockout
Proteínas dos Microfilamentos/genética
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actin Depolymerizing Factors); 0 (Microfilament Proteins); 0 (Wdr1 protein, mouse); EC 2.7.11.1 (Lim Kinases); EC 2.7.11.1 (Limk1 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.759886


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[PMID]:27986432
[Au] Autor:Li J; Liu Y; Jin Y; Wang R; Wang J; Lu S; VanBuren V; Dostal DE; Zhang SL; Peng X
[Ad] Endereço:Department of Medical Physiology, College of Medicine, Texas A&M University, USA.
[Ti] Título:Essential role of Cdc42 in cardiomyocyte proliferation and cell-cell adhesion during heart development.
[So] Source:Dev Biol;421(2):271-283, 2017 Jan 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cell migration, proliferation, differentiation and survival. However, the role of Cdc42 in heart development remains largely unknown. To determine the function of Cdc42 in heart formation, we have generated a Cdc42 cardiomyocyte knockout (CCKO) mouse line by crossing Cdc42 flox mice with myosin light chain (MLC) 2a-Cre mice. The inactivation of Cdc42 in embryonic cardiomyocytes induced lethality after embryonic day 12.5. Histological analysis of CCKO embryos showed cardiac developmental defects that included thin ventricular walls and ventricular septum defects. Microarray and real-time PCR data also revealed that the expression level of p21 was significantly increased and cyclin B1 was dramatically decreased, suggesting that Cdc42 is required for cardiomyocyte proliferation. Phosphorylated Histone H3 staining confirmed that the inactivation of Cdc42 inhibited cardiomyocytes proliferation. In addition, transmission electron microscope studies showed disorganized sarcomere structure and disruption of cell-cell contact among cardiomyocytes in CCKO hearts. Accordingly, we found that the distribution of N-cadherin/ß-Catenin in CCKO cardiomyocytes was impaired. Taken together, our data indicate that Cdc42 is essential for cardiomyocyte proliferation, sarcomere organization and cell-cell adhesion during heart development.
[Mh] Termos MeSH primário: Coração/embriologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Proteína cdc42 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Caderinas/metabolismo
Adesão Celular
Comunicação Celular
Membrana Celular/metabolismo
Proliferação Celular
Células Cultivadas
Perda do Embrião/patologia
Embrião de Mamíferos/metabolismo
Embrião de Mamíferos/patologia
Deleção de Genes
Regulação da Expressão Gênica no Desenvolvimento
Comunicação Interventricular/embriologia
Comunicação Interventricular/patologia
Camundongos Knockout
Miócitos Cardíacos/ultraestrutura
Especificidade de Órgãos
Transporte Proteico
beta Catenina/metabolismo
Proteína cdc42 de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (beta Catenin); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161218
[St] Status:MEDLINE



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