ArticleScientific reports2017
Progesterone Via its Type-A Receptor Promotes Myometrial Gap Junction Coupling.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- The hormonal control of parturition.Physiological reviews · 2024Review
- Progesterone inactivation in decidual stromal cells: A mechanism for inflammation-induced parturition.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Integrative analysis of noncoding mutations identifies the druggable genome in preterm birth.Science advances · 2024Article
- Challenges in Using Progestin to Prevent Singleton Preterm Births: Current Knowledge and Clinical Advice.International journal of women's health · 2024Review
- Review
- β3 Receptor Signaling in Pregnant Human Myometrium Suggests a Role for β3 Agonists as Tocolytics.Biomolecules · 2023Review
- Article
- In Vivo Genome-Wide PGR Binding in Pregnant Human Myometrium Identifies Potential Regulators of Labor.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- The selective progesterone receptor modulator-promegestone-delays term parturition and prevents systemic inflammation-mediated preterm birth in mice.American journal of obstetrics and gynecology · 2022Article
- Spontaneous preterm birth: Involvement of multiple feto-maternal tissues and organ systems, differing mechanisms, and pathways.Frontiers in endocrinology · 2022Review
- Nuclear Receptors in Pregnancy and Outcomes: Clinical Perspective.Advances in experimental medicine and biology · 2022Article
- Article
- Pro-inflammatory signals induce 20α-HSD expression in myometrial cells: A key mechanism for local progesterone withdrawal.Journal of cellular and molecular medicine · 2021Article
- Next generation strategies for preventing preterm birth.Advanced drug delivery reviews · 2021Review
- Landscape of Preterm Birth Therapeutics and a Path Forward.Journal of clinical medicine · 2021Review
- Transcriptional control of parturition: insights from gene regulation studies in the myometrium.Molecular human reproduction · 2021Review
- Enhanced drug delivery to the reproductive tract using nanomedicine reveals therapeutic options for prevention of preterm birth.Science translational medicine · 2021Article
- Inflammatory Amplification: A Central Tenet of Uterine Transition for Labor.Frontiers in cellular and infection microbiology · 2021Review
- Auxiliary trafficking subunit GJA1-20k protects connexin-43 from degradation and limits ventricular arrhythmias.The Journal of clinical investigation · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Effective labour contractions require synchronization of myometrial cells through gap junctions (GJs). Clasically, progesterone (P4) is known to inhibit the expression of connexin-43 (Cx43, major component of GJs) and GJ formation in myometrium. Our current study is based on a striking observation that challenges this dogma. We observed conspicuous differences in the intracellular localization of Cx43 protein in PRA versus PRB expressing myocytes. Thus in P4 stimulated PRA cells Cx43 protein forms GJs, whereas in PRB cells the forward trafficking of Cx43 and GJ formation is inhibited even when Cx43 is overexpressed. We found that P4, via PRA/B, differentially regulates Cx43 translation to generate a Cx43-20 K isoform, which facilitates the transport of full length Cx43 to plasma membrane. The P4 mediated regulation of Cx43 trafficking and GJ formation occurs via non-genomic pathway and involves the regulation of mTOR signaling since inhibition of this pathway restored the Cx43 trafficking defect in PRB cells. We propose that PRA is a master regulator of Cx43 expression, GJ formation and myocyte connectivity/synchronization for labour.
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.