1. Mitochondria Transfer from Adipose Stem Cells Improves the Developmental Potential of Cryopreserved Oocytes.
期刊:Biomolecules
日期:2022-07-21
DOI :10.3390/biom12071008
Although it is not a well-established technology, oocyte cryopreservation is becoming prevalent in assisted reproductive technologies in response to the growing demands of patients' sociological and pathological conditions. Oocyte cryopreservation can adversely affect the developmental potential of oocytes by causing an increase in intracellular oxidative stresses and damage to the mitochondrial structure. In this study, we studied whether autologous adipose stem cell (ASC) mitochondria supplementation with vitrified and warmed oocytes could restore post-fertilization development that decreased due to mitochondrial damage following cryopreservation. ASC mitochondria showed similar morphology to oocytes' mitochondria and had a higher ATP production capacity. The vitrified-warmed oocytes from juvenile mice were supplemented with ASC mitochondria at the same time as intracellular sperm injection (ICSI), after which we compared their developmental capacity and the mitochondria quality of 2-cell embryos. We found that, compared to their counterpart, mitochondria supplementation significantly improved development from 2-cell embryos to blastocysts (56.8% vs. 38.2%) and ATP production in 2-cell embryos (905.6 & 561.1 pmol), while reactive oxygen species levels were comparable. With these results, we propose that ASC mitochondria supplementation could restore the quality of cryopreserved oocytes and enhance the embryo developmental capacity, signifying another possible approach for mitochondrial transplantation therapy.
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2区Q1影响因子: 7.5
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2. Fetal and obstetrics manifestations of mitochondrial diseases.
期刊:Journal of translational medicine
日期:2024-09-23
DOI :10.1186/s12967-024-05633-6
During embryonic and neonatal development, mitochondria have essential effects on metabolic and energetic regulation, shaping cell fate decisions and leading to significant short- and long-term effects on embryonic and offspring health. Therefore, perturbation on mitochondrial function can have a pathological effect on pregnancy. Several shreds of evidence collected in preclinical models revealed that severe mitochondrial dysfunction is incompatible with life or leads to critical developmental defects, highlighting the importance of correct mitochondrial function during embryo-fetal development. The mechanism impairing the correct development is unknown and may include a dysfunctional metabolic switch in differentiating cells due to decreased ATP production or altered apoptotic signalling. Given the central role of mitochondria in embryonic and fetal development, the mitochondrial dysfunction typical of Mitochondrial Diseases (MDs) should, in principle, be detectable during pregnancy. However, little is known about the clinical manifestations of MDs in embryonic and fetal development. In this manuscript, we review preclinical and clinical evidence suggesting that MDs may affect fetal development and highlight the fetal and maternal outcomes that may provide a wake-up call for targeted genetic diagnosis.
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3. Development and Functions of Mitochondria in Early Life.
期刊:Newborn (Clarksville, Md.)
日期:2022 Jan-Mar
DOI :10.5005/jp-journals-11002-0013
Mitochondria are highly dynamic organelles of bacterial origin in eukaryotic cells. These play a central role in metabolism and adenosine triphosphate (ATP) synthesis and in the production and regulation of reactive oxygen species (ROS). In addition to the generation of energy, mitochondria perform numerous other functions to support key developmental events such as fertilization during reproduction, oocyte maturation, and the development of the embryo. During embryonic and neonatal development, mitochondria may have important effects on metabolic, energetic, and epigenetic regulation, which may have significant short- and long-term effects on embryonic and offspring health. Hence, the environment, epigenome, and early-life regulation are all linked by mitochondrial integrity, communication, and metabolism.
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2区Q1影响因子: 3.7
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4. DOHaD: A Menagerie of Adaptations and Perspectives: The interplay between early embryo metabolism and mitoepigenetic programming of development.
期刊:Reproduction (Cambridge, England)
日期:2023-05-25
DOI :10.1530/REP-22-0424
In brief:This review discusses advances in the knowledge of epigenetic mechanisms regulating mitochondrial DNA and the relationship with reproductive biology. Abstract:Initially perceived simply as an ATP producer, mitochondria also participate in a wide range of other cellular functions. Mitochondrial communication with the nucleus, as well as signaling to other cellular compartments, is critical to cell homeostasis. Therefore, during early mammalian development, mitochondrial function is reported as a key element for survival. Any mitochondrial dysfunction may reflect in poor oocyte quality and may impair embryo development with possible long-lasting consequences to cell functions and the overall embryo phenotype. Growing evidence suggests that the availability of metabolic modulators can alter the landscape of epigenetic modifications in the nuclear genome providing an important layer for the regulation of nuclear-encoded gene expression. However, whether mitochondria could also be subjected to such similar epigenetic alterations and the mechanisms involved remain largely obscure and controversial. Mitochondrial epigenetics, also known as 'mitoepigenetics' is an intriguing regulatory mechanism in mitochondrial DNA (mtDNA)-encoded gene expression. In this review, we summarized the recent advances in mitoepigenetics, with a special focus on mtDNA methylation in reproductive biology and preimplantation development. A better comprehension of the regulatory role of mitoepigenetics will help the understanding of mitochondrial dysfunction and provide novel strategies for in vitro production systems and assisted reproduction technologies, as well as prevent metabolic related stress and diseases.
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2区Q1影响因子: 3.7
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5. Mitochondria in early development: linking the microenvironment, metabolism and the epigenome.
作者:Harvey Alexandra J
期刊:Reproduction (Cambridge, England)
日期:2019-05-01
DOI :10.1530/REP-18-0431
Mitochondria, originally of bacterial origin, are highly dynamic organelles that have evolved a symbiotic relationship within eukaryotic cells. Mitochondria undergo dynamic, stage-specific restructuring and redistribution during oocyte maturation and preimplantation embryo development, necessary to support key developmental events. Mitochondria also fulfil a wide range of functions beyond ATP synthesis, including the production of intracellular reactive oxygen species and calcium regulation, and are active participants in the regulation of signal transduction pathways. Communication between not only mitochondria and the nucleus, but also with other organelles, is emerging as a critical function which regulates preimplantation development. Significantly, perturbations and deficits in mitochondrial function manifest not only as reduced quality and/or poor oocyte and embryo development but contribute to post-implantation failure, long-term cell function and adult disease. A growing body of evidence indicates that altered availability of metabolic co-factors modulate the activity of epigenetic modifiers, such that oocyte and embryo mitochondrial activity and dynamics have the capacity to establish long-lasting alterations to the epigenetic landscape. It is proposed that preimplantation embryo development may represent a sensitive window during which epigenetic regulation by mitochondria is likely to have significant short- and long-term effects on embryo, and offspring, health. Hence, mitochondrial integrity, communication and metabolism are critical links between the environment, the epigenome and the regulation of embryo development.
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2区Q1影响因子: 3.7
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6. OXIDATIVE STRESS AND REPRODUCTIVE FUNCTION: Reactive oxygen species in the mammalian pre-implantation embryo.
期刊:Reproduction (Cambridge, England)
日期:2022-10-26
DOI :10.1530/REP-22-0121
In brief:Reactive oxygen species are generated throughout the pre-implantation period and are necessary for normal embryo formation. However, at pathological levels, they result in reduced embryo viability which can be mediated through factors delivered by sperm and eggs at conception or from the external environment. Abstract:Reactive oxygen species (ROS) occur naturally in pre-implantation embryos as a by-product of ATP generation through oxidative phosphorylation and enzymes such as NADPH oxidase and xanthine oxidase. Biological concentrations of ROS are required for crucial embryonic events such as pronuclear formation, first cleavage and cell proliferation. However, high concentrations of ROS are detrimental to embryo development, resulting in embryo arrest, increased DNA damage and modification of gene expression leading to aberrant fetal growth and health. In vivo embryos are protected against oxidative stress by oxygen scavengers present in follicular and oviductal fluids, while in vitro, embryos rely on their own antioxidant defence mechanisms to protect against oxidative damage, including superoxide dismutase, catalase, glutathione and glutamylcysteine synthestase. Pre-implantation embryonic ROS originate from eggs, sperm and embryos themselves or from the external environment (i.e. in vitro culture system, obesity and ageing). This review examines the biological and pathological roles of ROS in the pre-implantation embryo, maternal and paternal origins of embryonic ROS, and from a clinical perspective, we comment on the growing interest in combating increased oxidative damage in the pre-implantation embryo through the addition of antioxidants.
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2区Q2影响因子: 5.2
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7. The Role of Mitochondria in Human Fertility and Early Embryo Development: What Can We Learn for Clinical Application of Assessing and Improving Mitochondrial DNA?
期刊:Cells
日期:2022-02-24
DOI :10.3390/cells11050797
Mitochondria are well known as 'the powerhouses of the cell'. Indeed, their major role is cellular energy production driven by both mitochondrial and nuclear DNA. Such a feature makes these organelles essential for successful fertilisation and proper embryo implantation and development. Generally, mitochondrial DNA is exclusively maternally inherited; oocyte's mitochondrial DNA level is crucial to provide sufficient ATP content for the developing embryo until the blastocyst stage of development. Additionally, human fertility and early embryogenesis may be affected by either point mutations or deletions in mitochondrial DNA. It was suggested that their accumulation may be associated with ovarian ageing. If so, is mitochondrial dysfunction the cause or consequence of ovarian ageing? Moreover, such an obvious relationship of mitochondria and mitochondrial genome with human fertility and early embryo development gives the field of mitochondrial research a great potential to be of use in clinical application. However, even now, the area of assessing and improving DNA quantity and function in reproductive medicine drives many questions and uncertainties. This review summarises the role of mitochondria and mitochondrial DNA in human reproduction and gives an insight into the utility of their clinical use.
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2区Q1影响因子: 6.6
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8. Mitochondrial Dysfunction and Oxidative Stress Caused by Cryopreservation in Reproductive Cells.
Mitochondria, fundamental organelles in cell metabolism, and ATP synthesis are responsible for generating reactive oxygen species (ROS), calcium homeostasis, and cell death. Mitochondria produce most ROS, and when levels exceed the antioxidant defenses, oxidative stress (OS) is generated. These changes may eventually impair the electron transport chain, resulting in decreased ATP synthesis, increased ROS production, altered mitochondrial membrane permeability, and disruption of calcium homeostasis. Mitochondria play a key role in the gamete competence to facilitate normal embryo development. However, iatrogenic factors in assisted reproductive technologies (ART) may affect their functional competence, leading to an abnormal reproductive outcome. Cryopreservation, a fundamental technology in ART, may compromise mitochondrial function leading to elevated intracellular OS that decreases sperm and oocytes' competence and the dynamics of fertilization and embryo development. This article aims to review the role played by mitochondria and ROS in sperm and oocyte function and the close, biunivocal relationships between mitochondrial damage and ROS generation during cryopreservation of gametes and gonadal tissues in different species. Based on current literature, we propose tentative hypothesis of mechanisms involved in cryopreservation-associated mitochondrial dysfunction in gametes, and discuss the role played by antioxidants and other agents to retain the competence of cryopreserved reproductive cells and tissues.
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4区Q4影响因子: 1.7
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9. Mitochondrial dynamics and interorganellar communication in the development and dysmorphism of mammalian oocytes.
作者:Udagawa Osamu , Ishihara Naotada
期刊:Journal of biochemistry
日期:2020-03-01
DOI :10.1093/jb/mvz093
Mitochondria play many critical roles in cells, not only by supplying energy, but also by supplying metabolites, buffering Ca2+ levels and regulating apoptosis. During oocyte maturation and subsequent embryo development, mitochondria change their morphology by membrane fusion and fission, and coordinately undergo multiple cellular events with the endoplasmic reticulum (ER) closely apposed. Mitochondrial fusion and fission, known as mitochondrial dynamics, are regulated by family members of dynamin GTPases. Oocytes in animal models with these regulators artificially altered exhibit morphological abnormalities in nearby mitochondria and at the ER interface that are reminiscent of major cytoplasmic dysmorphisms in human assisted reproductive technology, in which a portion of mature oocytes retrieved from patients contain cytoplasmic dysmorphisms associated with mitochondria and ER abnormal morphologies. Understanding organelle morpho-homeostasis in oocytes obtained from animal models will contribute to the development of novel methods for determining oocyte health and for how to deal with dysmorphic oocytes.
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2区Q2影响因子: 3.6
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10. The first cell-fate decision of mouse preimplantation embryo development: integrating cell position and polarity.
作者:Mihajlović Aleksandar I , Bruce Alexander W
期刊:Open biology
日期:2017-11-01
DOI :10.1098/rsob.170210
During the first cell-fate decision of mouse preimplantation embryo development, a population of outer-residing polar cells is segregated from a second population of inner apolar cells to form two distinct cell lineages: the trophectoderm and the inner cell mass (ICM), respectively. Historically, two models have been proposed to explain how the initial differences between these two cell populations originate and ultimately define them as the two stated early blastocyst stage cell lineages. The 'positional' model proposes that cells acquire distinct fates based on differences in their relative position within the developing embryo, while the 'polarity' model proposes that the differences driving the lineage segregation arise as a consequence of the differential inheritance of factors, which exhibit polarized subcellular localizations, upon asymmetric cell divisions. Although these two models have traditionally been considered separately, a growing body of evidence, collected over recent years, suggests the existence of a large degree of compatibility. Accordingly, the main aim of this review is to summarize the major historical and more contemporarily identified events that define the first cell-fate decision and to place them in the context of both the originally proposed positional and polarity models, thus highlighting their functional complementarity in describing distinct aspects of the developmental programme underpinning the first cell-fate decision in mouse embryogenesis.
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2区Q1影响因子: 3.5
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11. Building Principles for Constructing a Mammalian Blastocyst Embryo.
作者:Pfeffer Peter L
期刊:Biology
日期:2018-07-23
DOI :10.3390/biology7030041
The self-organisation of a fertilised egg to form a blastocyst structure, which consists of three distinct cell lineages (trophoblast, epiblast and hypoblast) arranged around an off-centre cavity, is unique to mammals. While the starting point (the zygote) and endpoint (the blastocyst) are similar in all mammals, the intervening events have diverged. This review examines and compares the descriptive and functional data surrounding embryonic gene activation, symmetry-breaking, first and second lineage establishment, and fate commitment in a wide range of mammalian orders. The exquisite detail known from mouse embryogenesis, embryonic stem cell studies and the wealth of recent single cell transcriptomic experiments are used to highlight the building principles underlying early mammalian embryonic development.
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3区Q1影响因子: 3.9
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12. Asynchronous division at 4-8-cell stage of preimplantation embryos affects live birth through ICM/TE differentiation.
期刊:Scientific reports
日期:2022-06-07
DOI :10.1038/s41598-022-13646-8
To improve the performance of assisted reproductive technology, it is necessary to find an indicator that can identify and select embryos that will be born or be aborted. We searched for indicators of embryo selection by comparing born/abort mouse embryos. We found that asynchronous embryos during the 4-8-cell stage were predisposed to be aborted. In asynchronous mouse embryos, the nuclear translocation of YAP1 in some blastomeres and compaction were delayed, and the number of ICMs was reduced. Hence, it is possible that asynchronous embryos have abnormal differentiation. When the synchrony of human embryos was observed, it was confirmed that embryos that did not reach clinical pregnancy had asynchrony as in mice. This could make synchrony a universal indicator common to all animal species.
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1区Q1影响因子: 90.2
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13. How embryos sort themselves out.
期刊:Nature reviews. Molecular cell biology
日期:2023-12-01
DOI :10.1038/s41580-023-00636-5
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3区Q1影响因子: 4.9
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14. Mitochondrial Transfer into Human Oocytes Improved Embryo Quality and Clinical Outcomes in Recurrent Pregnancy Failure Cases.
期刊:International journal of molecular sciences
日期:2023-02-01
DOI :10.3390/ijms24032738
One of the most critical issues to be solved in reproductive medicine is the treatment of patients with multiple failures of assisted reproductive treatment caused by low-quality embryos. This study investigated whether mitochondrial transfer to human oocytes improves embryo quality and provides subsequent acceptable clinical results and normality to children born due to the use of this technology. We transferred autologous mitochondria extracted from oogonia stem cells to mature oocytes with sperm at the time of intracytoplasmic sperm injection in 52 patients with recurrent failures (average 5.3 times). We assessed embryo quality using the following three methods: good-quality embryo rates, transferable embryo rates, and a novel embryo-scoring system (embryo quality score; EQS) in 33 patients who meet the preset inclusion criteria for analysis. We also evaluated the clinical outcomes of the in vitro fertilization and development of children born using this technology and compared the mtDNA sequences of the children and their mothers. The good-quality embryo rates, transferable embryo rates, and EQS significantly increased after mitochondrial transfer and resulted in 13 babies born in normal conditions. The mtDNA sequences were almost identical to the respective maternal sequences at the 83 major sites examined. Mitochondrial transfer into human oocytes is an effective clinical option to enhance embryo quality in recurrent in vitro fertilization-failure cases.
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2区Q2影响因子: 3
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15. Oocyte mitochondria-key regulators of oocyte function and potential therapeutic targets for improving fertility.
期刊:Biology of reproduction
日期:2022-02-22
DOI :10.1093/biolre/ioac024
The development of oocytes and early embryos is dependent on mitochondrial ATP production. This reliance on mitochondrial activity, together with the exclusively maternal inheritance of mitochondria in development, places mitochondria as central regulators of both fertility and transgenerational inheritance mechanisms. Mitochondrial mass and mtDNA content massively increase during oocyte growth. They are highly dynamic organelles and oocyte maturation is accompanied by mitochondrial trafficking around subcellular compartments. Due to their key roles in generation of ATP and reactive oxygen species (ROS), oocyte mitochondrial defects have largely been linked with energy deficiency and oxidative stress. Pharmacological treatments and mitochondrial supplementation have been proposed to improve oocyte quality and fertility by enhancing ATP generation and reducing ROS levels. More recently, the role of mitochondria-derived metabolites in controlling epigenetic modifiers has provided a mechanistic basis for mitochondria-nuclear crosstalk, allowing adaptation of gene expression to specific metabolic states. Here, we discuss the multi-faceted mechanisms by which mitochondrial function influence oocyte quality, as well as longer-term developmental events within and across generations.
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1区Q1影响因子: 4.4
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16. Symposium review: Reduction in oocyte developmental competence by stress is associated with alterations in mitochondrial function.
作者:Roth Zvi
期刊:Journal of dairy science
日期:2018-02-01
DOI :10.3168/jds.2017-13389
Stress can affect reproductive performance of lactating cows by targeting the ovarian pool of follicles and their enclosed oocytes. Among the documented stressors are heat stress (i.e., high temperature-humidity index) as well as environmental and food toxins. Oocytes collected during the hot season are of lower quality than those collected in the winter, expressed by reduced oocyte maturation and developmental competence. A similar pattern has been reported for oocytes exposed to endocrine-disrupting chemicals. Whereas the underlying mechanism might differ among stressors, accumulating evidence suggests that stress-induced impairment of oocyte developmental competence involves alterations in mitochondrial functioning. Within the oocyte, mitochondria are involved in ATP generation, calcium homeostasis, regulation of cytoplasmic reduction-oxidation, signal transduction, and apoptosis. Summer heat stress is strongly associated with alterations in mitochondrial distribution and alterations in mitochondria membrane potential. Heat stress impairs the expression of mitochondrion-associated genes, in particular those related to mitochondrial DNA transcription and replication and encoding oxidative phosphorylation complexes for ATP production. Reduction of ATP levels below the required threshold is suggested to compromise the progression of oocyte maturation and, subsequently, embryonic development. Another mechanism associated with mitochondrial function is the increase in reactive oxygen species (ROS), which has been documented in oocytes exposed to heat stress or environmental toxicants. Oxidative phosphorylation in mitochondria is the major source of ROS. Under physiological conditions, ROS are essential for nuclear maturation; however, disequilibrium between ROS production and antioxidative capacity might lead to DNA damage and apoptosis. The current review provides new insights into the oocyte's cellular and molecular responses to stress with an emphasis on the mitochondria. It discusses some strategies to mitigate the effects of stress on the mitochondria, such as incorporation of coenzyme Q10-a key component of the mitochondrial respiratory chain-administration of antioxidants, and injection of healthy mitochondria. Exploring the oocyte's cellular and molecular responses, in particular that of the mitochondria, might lead to the development of new strategies to mitigate the effects of various stressors on fertility.
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17. Mitochondrial Dynamics during Development.
期刊:Newborn (Clarksville, Md.)
日期:2023-04-06
DOI :10.5005/jp-journals-11002-0053
Mitochondria are dynamic membrane-bound organelles in eukaryotic cells. These are important for the generation of chemical energy needed to power various cellular functions and also support metabolic, energetic, and epigenetic regulation in various cells. These organelles are also important for communication with the nucleus and other cellular structures, to maintain developmental sequences and somatic homeostasis, and for cellular adaptation to stress. Increasing information shows mitochondrial defects as an important cause of inherited disorders in different organ systems. In this article, we provide an extensive review of ontogeny, ultrastructural morphology, biogenesis, functional dynamics, important clinical manifestations of mitochondrial dysfunction, and possibilities for clinical intervention. We present information from our own clinical and laboratory research in conjunction with information collected from an extensive search in the databases PubMed, EMBASE, and Scopus.
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1区Q1影响因子: 7
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18. Updates on preimplantation embryo research.
期刊:Fertility and sterility
日期:2023-05-06
DOI :10.1016/j.fertnstert.2023.04.039
Preimplantation development is the only stage of human development that can be studied outside the body in real time, as human embryos can be produced by in vitro fertilization and cultured in the laboratory as self-contained structures until the blastocyst stage. Here, we focus some of the key cellular and morphogenetic processes by which the 1-cell embryo is transformed gradually into a blastocyst ready for implantation. Although most of our knowledge about the dynamic series of events patterning preimplantation human development derives from work in mouse embryos, we discuss key differences that could exist with humans. Furthermore, we highlight how new approaches may enable to reveal many of the unknown processes driving human preimplantation development, particularly using noninvasive imaging and genetic technologies.
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2区Q1影响因子: 6
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19. Morphogenesis of the human preimplantation embryo: bringing mechanics to the clinics.
作者:Firmin Julie , Maître Jean-Léon
期刊:Seminars in cell & developmental biology
日期:2021-07-10
DOI :10.1016/j.semcdb.2021.07.005
During preimplantation development, the human embryo forms the blastocyst, the structure enabling uterine implantation. The blastocyst consists of an epithelial envelope, the trophectoderm, encompassing a fluid-filled lumen, the blastocoel, and a cluster of pluripotent stem cells, the inner cell mass. This specific architecture is crucial for the implantation and further development of the human embryo. Furthermore, the morphology of the human embryo is a prime determinant for clinicians to assess the implantation potential of in vitro fertilized human embryos, which constitutes a key aspect of assisted reproduction technology. Therefore, it is crucial to understand how the human embryo builds the blastocyst. As any material, the human embryo changes shape under the action of forces. Here, we review recent advances in our understanding of the mechanical forces shaping the blastocyst. We discuss the cellular processes responsible for generating morphogenetic forces that were studied mostly in the mouse and review the literature on human embryos to see which of them may be conserved. Based on the specific morphological defects commonly observed in clinics during human preimplantation development, we discuss how mechanical forces and their underlying cellular processes may be affected. Together, we propose that bringing tissue mechanics to the clinics will advance our understanding of human preimplantation development, as well as our ability to help infertile couples to have babies.
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2区Q1影响因子: 4.3
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20. Editorial: Molecular and cellular mechanisms in preimplantation IVF-embryo development.
期刊:Frontiers in cell and developmental biology
日期:2023-08-31
DOI :10.3389/fcell.2023.1279129
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3区Q1影响因子: 3.9
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21. Tripolar mitosis and partitioning of the genome arrests human preimplantation development in vitro.
作者:Ottolini Christian S , Kitchen John , Xanthopoulou Leoni , Gordon Tony , Summers Michael C , Handyside Alan H
期刊:Scientific reports
日期:2017-08-29
DOI :10.1038/s41598-017-09693-1
Following in vitro fertilisation (IVF), only about half of normally fertilised human embryos develop beyond cleavage and morula stages to form a blastocyst in vitro. Although many human embryos are aneuploid and genomically imbalanced, often as a result of meiotic errors inherited in the oocyte, these aneuploidies persist at the blastocyst stage and the reasons for the high incidence of developmental arrest remain unknown. Here we use genome-wide SNP genotyping and meiomapping of both polar bodies to identify maternal meiotic errors and karyomapping to fingerprint the parental chromosomes in single cells from disaggregated arrested embryos and excluded cells from blastocysts. Combined with time lapse imaging of development in culture, we demonstrate that tripolar mitoses in early cleavage cause chromosome dispersal to clones of cells with identical or closely related sub-diploid chromosome profiles resulting in intercellular partitioning of the genome. We hypothesise that following zygotic genome activation (ZGA), the combination of genomic imbalance and partial genome loss disrupts the normal pattern of embryonic gene expression blocking development at the morula-blastocyst transition. Failure to coordinate the cell cycle in early cleavage and regulate centrosome duplication is therefore a major cause of human preimplantation developmental arrest in vitro.
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2区Q1影响因子: 6
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22. The role of mitochondrial dynamics in oocyte and early embryo development.
期刊:Seminars in cell & developmental biology
日期:2024-02-08
DOI :10.1016/j.semcdb.2024.01.007
Mitochondrial dysfunction is widely implicated in various human diseases, through mechanisms that go beyond mitochondria's well-established role in energy generation. These dynamic organelles exert vital control over numerous cellular processes, including calcium regulation, phospholipid synthesis, innate immunity, and apoptosis. While mitochondria's importance is acknowledged in all cell types, research has revealed the exceptionally dynamic nature of the mitochondrial network in oocytes and embryos, finely tuned to meet unique needs during gamete and pre-implantation embryo development. Within oocytes, both the quantity and morphology of mitochondria can significantly change during maturation and post-fertilization. These changes are orchestrated by fusion and fission processes (collectively known as mitochondrial dynamics), crucial for energy production, content exchange, and quality control as mitochondria adjust to the shifting energy demands of oocytes and embryos. The roles of proteins that regulate mitochondrial dynamics in reproductive processes have been primarily elucidated through targeted deletion studies in animal models. Notably, impaired mitochondrial dynamics have been linked to female reproductive health, affecting oocyte quality, fertilization, and embryo development. Dysfunctional mitochondria can lead to fertility problems and can have an impact on the success of pregnancy, particularly in older reproductive age women.