ArticleBiology of reproduction2020
Developmental programming: prenatal testosterone-induced epigenetic modulation and its effect on gene expression in sheep ovary†.
Article in Biology of reproduction, 2020. 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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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
21 citing papers in PubMed, 29 citations in OpenAlex.
- Prenatal Androgenization Modifies H3K9me3 Binding in the Promoter of the Androgen Receptor Gene in the Arcuate Nucleus of the Adult Female Mouse.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Molecular Mechanisms Underlying Reproductive Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- The Metabolic Role of Mitochondria in the Perinatal Cardiac Development and Cardiovascular Diseases.Exploration (Beijing, China) · 2026Review
- Regulation of ovarian function in domestic animals: translational insights into human ovarian dynamics and dysfunction.Frontiers in endocrinology · 2026Review
- PSVRP: a pig structural variant reference panel for complex trait genomics and precision breeding.BMC genomics · 2025Article
- POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Genetics of polycystic ovary syndrome (PCOS).Reproduction (Cambridge, England) · 2025Review
- Shared Pathophysiological Mechanisms and Genetic Factors in Early Menarche and Polycystic Ovary Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Polycystic Ovarian Syndrome: A Review of Multi-omics Analyses.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- The Influences of Perinatal Androgenic Exposure on Cardiovascular and Metabolic Disease of Offspring of PCOS.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Structural and functional changes in rat uterus induced by neonatal androgenization.Journal of molecular histology · 2022Article
- Ovarian expression of follicle stimulating hormone and activin receptors genes in a prenatally-androgenized rat model of polycystic ovary syndrome in adulthood.Molecular biology reports · 2022Article
- Jumonji Domain-containing Protein-3 (JMJD3/Kdm6b) Is Critical for Normal Ovarian Function and Female Fertility.Endocrinology · 2022Article
- Posttranslational modifications in pathogenesis of PCOS.Frontiers in endocrinology · 2022Review
- Androgen-induced epigenetic modulations in the ovary.The Journal of endocrinology · 2021Review
- Sex- and Gender-Based Pharmacological Response to Drugs.Pharmacological reviews · 2021Article
- Androgens regulate ovarian gene expression by balancing Ezh2-Jmjd3 mediated H3K27me3 dynamics.PLoS genetics · 2021Article
- Sex-Bias in Irritable Bowel Syndrome: Linking Steroids to the Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- Article
- Fate and functional roles of Prominin 1Scientific reports · 2020Article
- Polycystic Ovary Syndrome: A Brain Disorder Characterized by Eating Problems Originating during Puberty and Adolescence.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Maternal perturbations or sub-optimal conditions during fetal development can predispose the offspring to diseases in adult life. Animal and human studies show that prenatal androgen excess may be an underlying cause of polycystic ovary syndrome (PCOS) later in life. In women, PCOS is a common fertility disorder with comorbid metabolic dysfunction. Here, using a sheep model of PCOS phenotype, we elucidate the epigenetic changes induced by prenatal (30-90 day) testosterone (T) treatment and its effect on gene expression in fetal day 90 (D90) and adult year 2 (Y2) ovaries. RNA-seq study shows 65 and 99 differentially regulated genes in prenatal T-treated fetal and adult ovaries, respectively. Interestingly, there were no differences in gene inducing histone marks H3K27ac, H3K9ac, and H3K4me3 or in gene silencing marks, H3K27me3 and H3K9me3 in the fetal D90 ovaries of control and excess T-exposed fetuses. In contrast, except for H3K4me3 and H3K27me3, all the other histone marks were upregulated in the prenatal T-treated adult Y2 ovary. Chromatin immunoprecipitation (ChIP) studies in adult Y2 ovaries established a direct relationship between the epigenetic modifications with the upregulated and downregulated genes obtained from RNA-seq. Results show increased gene inducing marks, H3K27ac and H3K9ac, on the promoter region of upregulated genes while gene silencing mark, H3K9me3, was also significantly increased on the downregulated genes. This study provides a mechanistic insight into prenatal T-induced developmental programming and its effect on ovarian gene expression that may contribute to reproductive dysfunction and development of PCOS in adult life.
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Registered trials
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