ArticlePlacenta2015
Loss of inherited genomic imprints in mice leads to severe disruption in placental lipid metabolism.
Article in Placenta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 42 citations in OpenAlex.
- High estrogen during ovarian stimulation induced loss of maternal imprinted methylation that is essential for placental development via overexpression of TET2 in mouse oocytes.Cell communication and signaling : CCS · 2024Article
- Extracellular vesicle-mediated targeting strategies for long-term health benefits in gestational diabetes.Clinical science (London, England : 1979) · 2023Review
- Multigenerational diabetes mellitus.Frontiers in endocrinology · 2023Review
- Reply to Suresh.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- The link between gestational diabetes and cardiovascular diseases: potential role of extracellular vesicles.Cardiovascular diabetology · 2022Review
- Multi-Omics Approaches and Radiation on Lipid Metabolism in Toothed Whales.Life (Basel, Switzerland) · 2021Review
- Sildenafil augments fetal weight and placental adiponectin in gestational testosterone-induced glucose intolerant rats.Toxicology reports · 2021Article
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- Visualization of microbes by 16S in situ hybridization in term and preterm placentas without intraamniotic infection.American journal of obstetrics and gynecology · 2019Article
- Epigenetically regulated imprinted gene expression associated with IVF and infertility: possible influence of prenatal stress and depression.Journal of assisted reproduction and genetics · 2019Review
- Transcriptome analysis of rhesus monkey failed-to-mature oocytes: deficiencies in transcriptional regulation and cytoplasmic maturation of the oocyte mRNA population.Molecular human reproduction · 2018Article
- Partial Loss of Genomic Imprinting Reveals Important Roles for Kcnq1 and Peg10 Imprinted Domains in Placental Development.PloS one · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
introductionMonoallelic expression of imprinted genes is necessary for placental development and normal fetal growth. Differentially methylated domains (DMDs) largely determine the parental-specific monoallelic expression of imprinted genes. Maternally derived DNA (cytosine-5-) -methyltransferase 1o (DNMT1o) maintains DMDs during the eight-cell stage of development. DNMT1o-deficient mouse placentas have a generalized disruption of genomic imprints. Previous studies have demonstrated that DNMT1o deficiency alters placental morphology and broadens the embryonic weight distribution in late gestation. Lipids are critical for fetal growth. Thus, we assessed the impact of disrupted imprinting on placental lipids.
methodsLipids were quantified from DNMT1o-deficient mouse placentas and embryos at E17.5 using a modified Folch method. Expression of select genes critical for lipid metabolism was quantified with RT-qPCR. Mitochondrial morphology was assessed by TEM and mitochondrial aconitase and cytoplasmic citrate concentrations quantified. DMD methylation was determined by EpiTYPER.
resultsWe found that DNMT1o deficiency is associated with increased placental triacylglycerol levels. Neither fetal triacylglycerol concentrations nor expression of select genes that mediate placental lipid transport were different from wild type. Placental triacylglycerol accumulation was associated with impaired beta-oxidation and abnormal citrate metabolism with decreased mitochondrial aconitase activity and increased cytoplasmic citrate concentrations. Loss of methylation at the MEST DMD was strongly associated with placental triacylglycerol accumulation. DISCUSSION: A generalized disruption of genomic imprints leads to triacylglycerol accumulation and abnormal mitochondrial function. This could stem directly from a loss of methylation at a given DMD, such as MEST, or represent a consequence of abnormal placental development.
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