ArticleReproductive biology and endocrinology : RB&E2018
PAPP-A2 deficiency does not exacerbate the phenotype of a mouse model of intrauterine growth restriction.
Article in Reproductive biology and endocrinology : RB&E, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- PAPPA's role in female reproduction.Reproduction (Cambridge, England) · 2025Review
- Sex differences in placental structure and gene expression in ICR mice during embryonic development.Scientific reports · 2025Article
- Screening of Oxidative Stress-related Biomarkers and Antioxidant Drugs for Polycystic Ovary Syndrome Based on Bioinformatics and Molecular Docking.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Roles of chromosomal and gonadal sex in the fetal and placental responses to maternal food restriction in mice.Molecular human reproduction · 2025Article
- Development and validation of preeclampsia predictive models using key genes from bioinformatics and machine learning approaches.Frontiers in immunology · 2024Article
- Development and Validation of a Small for Gestational Age Screening Model at 21-24 Weeks Based on the Real-World Clinical Data.Journal of clinical medicine · 2023Article
- The Placenta's Role in Sexually Dimorphic Fetal Growth Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- Disorders caused by genetic defects associated with GH-dependent genes: PAPPA2 defects.Molecular and cellular endocrinology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPregnancy-associated plasma protein-A2 (PAPP-A2) is consistently upregulated in the placentae of pregnancies complicated by preeclampsia and fetal growth restriction. The causes and significance of this upregulation remain unknown, but it has been hypothesized that it is a compensatory response to improve placental growth and development. We predicted that, if the upregulation of PAPP-A2 in pregnancy complications reflects a compensatory response, then deletion of Pappa2 in mice would exacerbate the effects of a gene deletion previously reported to impair placental development: deficiency of matrix metalloproteinase-9 (MMP9).
methodsWe crossed mice carrying deletions in Pappa2 and Mmp9 to produce pregnancies deficient in one, both, or neither of these genes. We measured pregnancy rates, number of conceptuses, fetal and placental growth, and the histological structure of the placenta.
resultsWe found no evidence of reduced fertility, increased pregnancy loss, or increased fetal demise in Mmp9
conclusionsEffects of Mmp9 deficiency were not exacerbated by the deletion of Pappa2. Our results do not provide evidence that upregulation of placental PAPP-A2 represents a mechanism to compensate for impaired fetal growth.
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Registered trials
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