ArticleDisease models & mechanisms2014
Isolating the role of elevated Phlda2 in asymmetric late fetal growth restriction in mice.
Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Imprinted genes and the manipulation of parenting in mammals.Nature reviews. Genetics · 2023Review
- In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring.Experimental physiology · 2022Review
- Prenatal health behaviours as predictors of human placental lactogen levels.Frontiers in endocrinology · 2022Article
- Impact of Chronic Prenatal Stress on Maternal Neuroendocrine Function and Embryo and Placenta Development During Early-to-Mid-Pregnancy in Mice.Frontiers in physiology · 2022Article
- Maternal background alters the penetrance of growth phenotypes and sex-specific placental adaptation of offspring sired by alcohol-exposed males.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Placental endocrine insufficiency programs anxiety, deficits in cognition and atypical social behaviour in offspring.Human molecular genetics · 2021Article
- Genes and pathways associated with pregnancy loss in dairy cattle.Scientific reports · 2021Article
- Deletion of the ImprintedGenes · 2021Article
- Considering intrauterine location in a model of fetal growth restriction after maternal titanium dioxide nanoparticle inhalation.Frontiers in toxicology · 2021Article
- Modeling human epigenetic disorders in mice: Beckwith-Wiedemann syndrome and Silver-Russell syndrome.Disease models & mechanisms · 2020Review
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- Identification of the novel Ido1 imprinted locus and its potential epigenetic role in pregnancy loss.Human molecular genetics · 2019Article
- Maternal care boosted by paternal imprinting in mammals.PLoS biology · 2018Article
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- Increased dosage of the imprinted Ascl2 gene restrains two key endocrine lineages of the mouse Placenta.Developmental biology · 2016Article
- Lentivirus-mediated PHLDA2 overexpression inhibits trophoblast proliferation, migration and invasion, and induces apoptosis.International journal of molecular medicine · 2016Article
- Placental PHLDA2 expression is increased in cases of fetal growth restriction following reduced fetal movements.BMC medical genetics · 2016Article
- The imprinted Phlda2 gene modulates a major endocrine compartment of the placenta to regulate placental demands for maternal resources.Developmental biology · 2016Article
- Placental expression of imprinted genes varies with sampling site and mode of delivery.Placenta · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pleckstrin homology-like domain family A member 2 (PHLDA2) is a maternally expressed imprinted gene whose elevated expression has been linked to fetal growth restriction in a number of human studies. In mice, Phlda2 negatively regulates placental growth and limits the accumulation of placental glycogen. We previously reported that a three-copy transgene spanning the Phlda2 locus drove a fetal growth restriction phenotype late in gestation, suggesting a causative role for PHLDA2 in human growth restriction. However, in this mouse model, Phlda2 was overexpressed by fourfold, alongside overexpression of a second imprinted gene, Slc22a18. Here, we genetically isolate the role of Phlda2 in driving late fetal growth restriction in mice. We furthermore show that this Phlda2-driven growth restriction is asymmetrical, with a relative sparing of the brain, followed by rapid catch-up growth after birth, classic features of placental insufficiency. Strikingly, fetal growth restriction showed strain-specific differences, being apparent on the 129S2/SvHsd (129) genetic background and absent on the C57BL6 (BL6) background. A key difference between these two strains is the placenta. Specifically, BL6 placentae possess a more extensive endocrine compartment and substantially greater stores of placental glycogen. Taken together, these data support a direct role for elevated Phlda2 in limiting fetal growth but also suggest that growth restriction only manifests when there is limited placental reserve. These findings should be taken into account in interpreting the results from human studies.
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