ArticlePloS one2013
Loss of progesterone receptor-mediated actions induce preterm cellular and structural remodeling of the cervix and premature birth.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- Cervical pessary to prevent preterm birth in asymptomatic high-risk women: a systematic review and meta-analysis.American journal of obstetrics and gynecology · 2020Pooled it
- Vaginal progesterone for preventing preterm birth and adverse perinatal outcomes in singleton gestations with a short cervix: a meta-analysis of individual patient data.American journal of obstetrics and gynecology · 2018Pooled it
- Environmental and genetic risk factors for preterm birth: interplays with stressful events during pregnancy.Pediatric research · 2025Article
- Spectrum of Cervical Insufficiency: Management Strategies from Asymptomatic Shortening to Emergent Membrane Prolapse.Journal of clinical medicine · 2025Review
- M1 Macrophages Are a Source of IL-1α: A Driver of Progesterone Metabolism and Myometrial Contraction.Cells · 2025Article
- Progesterone regulation of cervix ripening in preterm and term birth in mice.Reproduction (Cambridge, England) · 2025Article
- Variants of the Progesterone Receptor Gene as Modulators of Risk for Idiopathic Spontaneous Premature Birth.International journal of molecular sciences · 2025Article
- Review
- Analysis of Vaginal Microbiota Variations in the Third Trimester of Pregnancy and Their Correlation with Preterm Birth: A Case-Control Study.Microorganisms · 2024Article
- Characteristic impairment of progesterone response in cultured cervical fibroblasts obtained from patients with refractory cervical insufficiency.Scientific reports · 2023Article
- Article
- Progesterone and its receptor signaling in cervical remodeling: Mechanisms of physiological actions and therapeutic implications.The Journal of steroid biochemistry and molecular biology · 2022Review
- Vaginal Nanoformulations for the Management of Preterm Birth.Pharmaceutics · 2022Review
- The effects of mifepristone on the structure of human decidua and chorion and Bax and Bcl-2 expression at early stage of pregnancy.BMC pharmacology & toxicology · 2022Article
- Heterogeneous microstructural changes of the cervix influence cervical funneling.Acta biomaterialia · 2022Article
- Progesterone alters human cervical epithelial and stromal cell transition and migration: Implications in cervical remodeling during pregnancy and parturition.Molecular and cellular endocrinology · 2021Article
- Article
- The pregnancy microbiome and preterm birth.Seminars in immunopathology · 2020Review
- Mechanics of cervical remodelling: insights from rodent models of pregnancy.Interface focus · 2019Review
- Effects of macrophage depletion on characteristics of cervix remodeling and pregnancy in CD11b-dtr mice.Biology of reproduction · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A decline in serum progesterone or antagonism of progesterone receptor function results in preterm labor and birth. Whether characteristics of premature remodeling of the cervix after antiprogestins or ovariectomy are similar to that at term was the focus of the present study. Groups of pregnant rats were treated with vehicle, a progesterone receptor antagonist (onapristone or mifepristone), or ovariectomized on day 17 postbreeding. As expected, controls given vehicle delivered at term while rats delivered preterm after progesterone receptor antagonist treatment or ovariectomy. Similar to the cervix before term, the preterm cervix of progesterone receptor antagonist-treated rats was characterized by reduced cell nuclei density, decreased collagen content and structure, as well as a greater presence of macrophages per unit area. Thus, loss of nuclear progesterone receptor-mediated actions promoted structural remodeling of the cervix, increased census of resident macrophages, and preterm birth much like that found in the cervix at term. In contrast to the progesterone receptor antagonist-induced advance in characteristics associated with remodeling, ovariectomy-induced loss of systemic progesterone did not affect hypertrophy, extracellular collagen, or macrophage numbers in the cervix. Thus, the structure and macrophage census in the cervix appear sufficient for premature ripening and birth to occur well before term. With progesterone receptors predominantly localized on cells other than macrophages, the findings suggest that interactions between cells may facilitate the loss of progesterone receptor-mediated actions as part of a final common mechanism that remodels the cervix in certain etiologies of preterm and with parturition at term.
Indexed as
Identifiers
What OpenQuestion holds
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.