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共9篇 平均IF=4.7 (2.6-14.6)更多分析
  • 1区Q1影响因子: 7
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    1. Oocyte maturation failure: a syndrome of bad eggs.
    期刊:Fertility and sterility
    日期:2010-04-07
    DOI :10.1016/j.fertnstert.2010.02.037
    To show that disruption of meiotic competence results in cell cycle arrest, and the production of immature oocytes that are not capable of fertilization. Through an extensive review of animal studies and clinical case reports, we define the syndrome of oocyte maturation failure as a distinct oocyte disorder, present a classification system based on clinical parameters, and discuss the potential molecular origins for the disease.
  • 1区Q1影响因子: 7
    2. Genes involved in recurrent oocyte maturation arrest: What do we know?
    作者:Segars James H , Diab Maya
    期刊:Fertility and sterility
    日期:2021-03-19
    DOI :10.1016/j.fertnstert.2021.02.043
  • 2区Q1影响因子: 6
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    3. Oocyte development, meiosis and aneuploidy.
    期刊:Seminars in cell & developmental biology
    日期:2015-10-08
    DOI :10.1016/j.semcdb.2015.10.005
    Meiosis is one of the defining events in gametogenesis. Male and female germ cells both undergo one round of meiotic cell division during their development in order to reduce the ploidy of the gametes, and thereby maintain the ploidy of the species after fertilisation. However, there are some aspects of meiosis in the female germline, such as the prolonged arrest in dictyate, that appear to predispose oocytes to missegregate their chromosomes and transmit aneuploidies to the next generation. These maternally-derived aneuploidies are particularly problematic in humans where they are major contributors to miscarriage, age-related infertility, and the high incidence of Down's syndrome in human conceptions. This review will discuss how events that occur in foetal oocyte development and during the oocytes' prolonged dictyate arrest can influence meiotic chromosome segregation and the incidence of aneuploidy in adult oocytes.
  • 2区Q1影响因子: 4.7
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    4. The art of oocyte meiotic arrest regulation.
    作者:Pan Bo , Li Julang
    期刊:Reproductive biology and endocrinology : RB&E
    日期:2019-01-05
    DOI :10.1186/s12958-018-0445-8
    A central dogma of mammalian reproductive biology is that the size of the primordial follicle pool represents reproductive capacity in females. The assembly of the primordial follicle starts after the primordial germ cells (PGCs)-derived oocyte releases from the synchronously dividing germline cysts. PGCs initiate meiosis during fetal development. However, after synapsis and recombination of homologous chromosomes, they arrest at the diplotene stage of the first meiotic prophase (MI). The diplotene-arrested oocyte, together with the surrounding of a single layer of flattened granulosa cells, forms a basic unit of the ovary, the primordial follicle. At the start of each estrous (animal) or menstrual cycle (human), in response to a surge of luteinizing hormone (LH) from the pituitary gland, a limited number of primordial follicles are triggered to develop into primary follicles, preantral follicles, antral follicles and reach to preovulatory follicle stage. During the transition from the preantral to antral stages, the enclosed oocyte gradually acquires the capacity to resume meiosis. Meiotic resumption from the prophase of MI is morphologically characterized by the dissolution of the oocyte nuclear envelope, which is generally termed the "germinal vesicle breakdown" (GVBD). Following GVBD and completion of MI, the oocyte enters meiosis II without an obvious S-phase and arrests at metaphase phase II (MII) until fertilization. The underlying mechanism of meiotic arrest has been widely explored in numerous studies. Many studies indicated that two cellular second messengers, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) play an essential role in maintaining oocyte meiotic arrest. This review will discuss how these two cyclic nucleotides regulate oocyte maturation by blocking or initiating meiotic processes, and to provide an insight in future research.
  • 2区Q1影响因子: 3.7
    5. Spindle assembly checkpoint-related meiotic defect in oocytes from LT/Sv mice has cytoplasmic origin and diminishes in older females.
    作者:Hoffmann Steffen , Król Marzena , Polanski Zbigniew
    期刊:Reproduction (Cambridge, England)
    日期:2012-06-26
    DOI :10.1530/REP-11-0362
    The spindle assembly checkpoint (SAC) ensures proper segregation of chromosomes by delaying anaphase onset until all kinetochores are properly attached to the spindle microtubules. Oocytes from the mouse strain LT/Sv arrest at the first meiotic metaphase (MI) due to, as reported recently, enormously prolonged activity of the SAC. We compared the dynamics of cyclin B1-GFP degradation, the process which is a measure of the SAC activity, in chromosomal and achromosomal halves of LT/Sv oocytes. In chromosome-containing oocyte halves arrested at MI, cyclin B1-GFP was not degraded indicating active SAC. However, in the halves lacking chromosomes, which is a condition precluding the SAC function, degradation always occurred confirming that MI arrest in LT/Sv oocytes is SAC dependent. Transferring the germinal vesicle (GV) from LT/Sv oocytes into the enucleated oocytes from wild-type mice resulted in the progression through meiosis one, indicating that a SAC-activating defect in LT/Sv oocytes is cytoplasmic, yet can be rescued by foreign cytoplasm. These results may help to define the etiology of the human infertility related to the oocyte MI arrest, indicating the involvement of the SAC as likely candidate, and point to GV transfer as the possible therapy. Finally, we found that majority of oocytes isolated from old LT/Sv mice complete the first meiosis. Reciprocal transfers of the GV between the oocytes from young and old LT/Sv females suggest that the factor(s) responsible for the reversal of the phenotype in oocytes from old mice is located both in the GV and in the cytoplasm.
  • 3区Q2影响因子: 2.6
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    6. A single bivalent efficiently inhibits cyclin B1 degradation and polar body extrusion in mouse oocytes indicating robust SAC during female meiosis I.
    作者:Hoffmann Steffen , Maro Bernard , Kubiak Jacek Z , Polanski Zbigniew
    期刊:PloS one
    日期:2011-11-18
    DOI :10.1371/journal.pone.0027143
    The Spindle Assembly Checkpoint (SAC) inhibits anaphase until microtubule-to-kinetochore attachments are formed, thus securing correct chromosome separation and preventing aneuploidy. Whereas in mitosis even a single unattached chromosome keeps the SAC active, the high incidence of aneuploidy related to maternal meiotic errors raises a concern about the lower efficiency of SAC in oocytes. Recently it was suggested that in mouse oocytes, contrary to somatic cells, not a single chromosome but a critical mass of chromosomes triggers efficient SAC pointing to the necessity of evaluating the robustness of SAC in oocytes. Two types of errors in chromosome segregation upon meiosis I related to SAC were envisaged: (1) SAC escape, when kinetochores emit SAC-activating signal unable to stop anaphase I; and (2) SAC deceive, when kinetochores do not emit the signal. Using micromanipulations and live imaging of the first polar body extrusion, as well as the dynamics of cyclin B1 degradation, here we show that in mouse oocytes a single bivalent keeps the SAC active. This is the first direct evaluation of SAC efficiency in mouse oocytes, which provides strong evidence that the robustness of SAC in mammalian oocytes is comparable to other cell types. Our data do not contradict the hypothesis of the critical mass of chromosomes necessary for SAC activation, but suggest that the same rule may govern SAC activity also in other cell types. We postulate that the innate susceptibility of oocytes to errors in chromosome segregation during the first meiotic division may not be caused by lower efficiency of SAC itself, but could be linked to high critical chromosome mass necessary to keep SAC active in oocyte of large size.
  • 2区Q2影响因子: 3
    7. Failure of meiotic competence in human oocytes.
    作者:Bar-Ami S , Zlotkin E , Brandes J M , Itskovitz-Eldor J
    期刊:Biology of reproduction
    日期:1994-05-01
    DOI :10.1095/biolreprod50.5.1100
    The administration of hCG to women undergoing in vitro fertilization and embryo transfer (IVF/ET) results in the meiotic maturation of cumulus-oocyte complexes (COC). Sometimes oocytes being aspirated for IVF/ET fail to resume meiosis in vivo and even after a subsequent 20-h incubation in vitro and are thus defined as meiotic competence failure (MCF) oocytes. The relationship between the proportion of MCF oocytes and other IVF/ET outcomes was studied over 3 years in 703 tested cycles of 487 women. Women yielding one or more MCF oocytes in at least one menstrual cycle represented 8.6% of this population and were defined as MCF women. Cumulus state in the MCF oocyte population was characterized as mature in 57.4 +/- 6.7%, intermediate in 13.9 +/- 4.0%, immature in 24.1 +/- 8.7%, and atretic in 4.6 +/- 2.7%. These values differed significantly, by 0.6-, 2.9-, 7.1-, and 4.6-fold, respectively, as compared to the corresponding COC aspirated from women yielding only meiotically competent (MC) oocytes. In a menstrual cycle yielding both MC and MCF oocytes, the IVF/ET variables were evaluated in the MC oocytes. Thus, in such cases the incidence of fertilization or cleavage and the number of blastomeres per embryo were significantly reduced concomitant with the increase in percentage of MCF oocytes. When the percentage of MCF oocytes was 25% or more, no pregnancy was achieved. Various follicular parameters and serum 17 beta-estradiol (E2) and progesterone (P4) levels were compared in MC and MCF women over the four days preceding day of aspiration.(ABSTRACT TRUNCATED AT 250 WORDS)
  • 3区Q3影响因子: 3.4
    8. Perturbation of survivin expression affects chromosome alignment and spindle checkpoint in mouse oocyte meiotic maturation.
    作者:Sun Shao-Chen , Wei Liang , Li Mo , Lin Sheng-Li , Xu Bao-Zeng , Liang Xing-Wei , Kim Nam-Hyung , Schatten Heide , Lu Sheng-Sheng , Sun Qing-Yuan
    期刊:Cell cycle (Georgetown, Tex.)
    日期:2009-10-19
    DOI :10.4161/cc.8.20.9855
    Survivin is a member of inhibitors of apoptosis proteins (IAPs), which have multiple regulatory functions in mitosis, but its roles in meiosis remain unknown. Here, we report its expression, localization and functions in mouse oocyte meiosis. Survivin displayed a maximal expression level in GV stage, and then gradually decreased from Pro-MI to MII stages. Immunofluorescent staining showed that survivin was restricted to the germinal vesicle, associated with centromeres from pro-metaphase I to metaphase I stages, distributed at the midzone and midbody of anaphase and telophase spindles, and located to centromeres at metaphase II stages. Depletion of survivin by antibody injection and morpholino injection resulted in severe chromosome misalignment, precocious polar body extrusion, and larger-than-normal polar bodies. Overexpression of survivin resulted in severe chromosome misalignment and prometaphase I or metaphase I arrest in a large proportion of oocytes. Our data suggest that survivin is required for chromosome alignment and that it may regulate spindle checkpoint activity during mouse oocyte meiosis.
  • 1区Q1影响因子: 14.6
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    9. A YAP/FOXM1 axis mediates EMT-associated EGFR inhibitor resistance and increased expression of spindle assembly checkpoint components.
    作者:Nilsson Monique B , Sun Huiying , Robichaux Jacqulyne , Pfeifer Matthias , McDermott Ultan , Travers Jon , Diao Lixia , Xi Yuanxin , Tong Pan , Shen Li , Hofstad Mia , Kawakami Masanori , Le Xiuning , Liu Xi , Fan Youhong , Poteete Alissa , Hu Limei , Negrao Marcelo V , Tran Hai , Dmitrovsky Ethan , Peng David , Gibbons Don L , Wang Jing , Heymach John V
    期刊:Science translational medicine
    日期:2020-09-02
    DOI :10.1126/scitranslmed.aaz4589
    Acquired resistance to tyrosine kinase inhibitors (TKIs) of epidermal growth factor receptor (EGFR) remains a clinical challenge. Especially challenging are cases in which resistance emerges through EGFR-independent mechanisms, such as through pathways that promote epithelial-to-mesenchymal transition (EMT). Through an integrated transcriptomic, proteomic, and drug screening approach, we identified activation of the yes-associated protein (YAP) and forkhead box protein M1 (FOXM1) axis as a driver of EMT-associated EGFR TKI resistance. EGFR inhibitor resistance was associated with broad multidrug resistance that extended across multiple chemotherapeutic and targeted agents, consistent with the difficulty of effectively treating resistant disease. EGFR TKI-resistant cells displayed increased abundance of spindle assembly checkpoint (SAC) proteins, including polo-like kinase 1 (PLK1), Aurora kinases, survivin, and kinesin spindle protein (KSP). Moreover, EGFR TKI-resistant cells exhibited vulnerability to SAC inhibitors. Increased activation of the YAP/FOXM1 axis mediated an increase in the abundance of SAC components in resistant cells. The clinical relevance of these finding was indicated by evaluation of specimens from patients with EGFR mutant lung cancer, which showed that high expression correlated with expression of genes encoding SAC proteins and was associated with a worse clinical outcome. These data revealed the YAP/FOXM1 axis as a central regulator of EMT-associated EGFR TKI resistance and that this pathway, along with SAC components, are therapeutic vulnerabilities for targeting this multidrug-resistant phenotype.
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