ArticleReproductive sciences (Thousand Oaks, Calif.)2012
HDAC1 and HDAC2 are differentially expressed in endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 82 citations in OpenAlex.
- Human Endometriosis Tissue Microarray Reveals Site-specific Expression of Estrogen Receptors, Progesterone Receptor, and Ki67.Applied immunohistochemistry & molecular morphology : AIMM · 2019Trial
- Research Progress of Histone Deacetylase and Its Inhibitors in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- HDAC3 Regulates Transcriptional Networks Governing Decidualization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Immune-epigenetic-metabolic crosstalk: attempting to unravel the multidimensional mechanisms of immune evasion in endometriosis.Frontiers in immunology · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- A role for gut mycobiome and altered fungal-bacterial interactions in women with endometriosis†.Biology of reproduction · 2025Article
- Precision Therapeutic and Preventive Molecular Strategies for Endometriosis-Associated Infertility.International journal of molecular sciences · 2025Review
- Exploring the molecular mechanism ofHeliyon · 2025Article
- Spatial transcriptomic analysis identifies epithelium-macrophage crosstalk in endometriotic lesions.iScience · 2025Article
- Endometrial Receptivity-Lessons from "Omics".Biomolecules · 2025Review
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs.Frontiers in genetics · 2025Review
- The roles of chromatin regulatory factors in endometriosis.Journal of assisted reproduction and genetics · 2024Review
- Epigallocatechin Gallate for the Treatment of Benign and Malignant Gynecological Diseases-Focus on Epigenetic Mechanisms.Nutrients · 2024Review
- A Systematic Review of Epigenetics of Endometriosis.F&S reviews · 2024Article
- Epigenetic Dysregulation in Endometriosis: Implications for Pathophysiology and Therapeutics.Endocrine reviews · 2023Review
- The Impact of Histone Modifications in Endometriosis Highlights New Therapeutic Opportunities.Cells · 2023Review
- Female reproductive dysfunctions and the gut microbiota.Journal of molecular endocrinology · 2022Review
- Epigenetic Factors in Eutopic Endometrium in Women with Endometriosis and Infertility.International journal of molecular sciences · 2022Review
- Endometriosis-associated infertility: From pathophysiology to tailored treatment.Frontiers in endocrinology · 2022Review
- Histone deacetylase HDAC2 silencing prevents endometriosis by activating the HNF4A/ARID1A axis.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Epigenetic mechanisms have been ascribed important roles in endometriosis. Covalent histone modifications at lysine residues have been shown to regulate gene expression and thus contribute to pathological states in many diseases. In endometriosis, histone deacetylase inhibition (HDACi) resulted in reactivation of E-cadherin, attenuation of invasion, decreased proliferation of endometriotic cells, and caused lesion regression in an animal model. This study was conducted to assess basal and hormone-regulated gene expression levels of HDAC1 and HDAC2 (HDAC1/2) in cell lines and protein expression levels in tissues. Basal and steroid hormone-regulated HDAC1/2 gene expression levels were determined by quantitative polymerase chain reaction in cell lines and tissues. Protein levels were measured by immunohistochemistry (IHC) in tissues on an endometriosis tissue microarray (TMA). Basal HDAC1/2 gene expression levels were significantly higher in endometriotic versus endometrial stromal cells, which was confirmed by Western blot analysis. Estradiol (E2) and progesterone (P4) significantly downregulated HDAC1 expression in endometrial epithelial cells. Levels of HDAC2 were upregulated by E2 and downregulated by E2 + P4 in endometrial stromal cells. Hormone modulation of HDAC1/2 gene expression was lost in the endometriotic cell line. Immunohistochemistry showed that HDAC1/2 proteins were expressed in a substantial proportion of lesions and endometrium from patients, and their expression levels varied according to lesion localization. The highest proportion of strong HDAC1 immunostaining was seen in ovarian, skin, and gastrointestinal lesions, and of HDAC2 in skin lesions and endometrium from patients with endometriosis. These studies suggest that endometriosis etiology may be partially explained by epigenetic regulation of gene expression due to dysregulations in the expression of HDACs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.