ArticleThe Journal of clinical endocrinology and metabolism2010
Altered retinoid uptake and action contributes to cell survival in endometriosis.
Article in The Journal of clinical endocrinology and metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Progesterone receptor ligands for the treatment of endometriosis: the mechanisms behind therapeutic success and failure.Human reproduction update · 2020Pooled it
- From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers.International journal of molecular sciences · 2025Review
- Endometriosis and ovulatory menstruation: beyond the Sampson principle.The Journal of clinical investigation · 2025Review
- Single-cell transcriptomic atlas of different endometriosis indicating that an interaction between endometriosis-associated mesothelial cells (EAMCs) and ectopic stromal cells may influence progesterone resistance.Clinical and translational medicine · 2025Article
- Epigenetic Dysregulation in Endometriosis: Implications for Pathophysiology and Therapeutics.Endocrine reviews · 2023Review
- Spheroids as a model for endometriotic lesions.JCI insight · 2023Article
- Gene expression of the endocannabinoid system in endometrium through menstrual cycle.Scientific reports · 2022Article
- Deficiency of RARα Suppresses DecidualizationFrontiers in endocrinology · 2022Article
- Obesity alters the ovarian proteomic response to zearalenone exposure†.Biology of reproduction · 2021Article
- Increased Expression of Retinol-Binding Protein 4 in Ovarian Endometrioma and Its Possible Role in the Pathogenesis of Endometriosis.International journal of molecular sciences · 2021Article
- Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review.Journal of clinical medicine · 2021Review
- Human Endometrial Stromal Cell Differentiation is Stimulated by PPARβ/δ Activation: New Targets for Infertility?The Journal of clinical endocrinology and metabolism · 2020Article
- Genetic, Epigenetic, and Steroidogenic Modulation Mechanisms in Endometriosis.Journal of clinical medicine · 2020Review
- Construction of a MicroRNA-mRNA Network Underlying Decidualized Endometriotic Cyst Stromal Cells Using Bioinformatics Analysis.BioMed research international · 2020Article
- Endometriosis.Endocrine reviews · 2019Review
- Endometriosis and nuclear receptors.Human reproduction update · 2019Review
- Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis.Frontiers in endocrinology · 2019Review
- Retinoid signaling controlled by SRC-2 in decidualization revealed by transcriptomicsReproduction (Cambridge, England) · 2018Article
- Retinoic acid regulates cell-shape and -death of E-FABP (FABP5)-immunoreactive septoclasts in the growth plate cartilage of mice.Histochemistry and cell biology · 2017Article
- KRAS Activation and over-expression of SIRT1/BCL6 Contributes to the Pathogenesis of Endometriosis and Progesterone Resistance.Scientific reports · 2017Article
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
contextRetinoic acid (RA) controls multiple biological processes via exerting opposing effects on cell survival. Retinol uptake into cells is controlled by stimulated by RA 6 (STRA6). RA is then produced from retinol in the cytosol. Partitioning of RA between the nuclear receptors RA receptor α and peroxisome-proliferator-activated receptor β/δ is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. The roles of these mechanisms in endometrium or endometriosis remain unknown.
objectiveThe aim was to determine the regulation of retinoid uptake and RA action in primary stromal cells from endometrium (n = 10) or endometriosis (n = 10).
resultsProgesterone receptor was necessary for high STRA6 and CRABP2 expression in endometrial stromal cells. STRA6, which was responsible for labeled retinoid uptake, was strikingly lower in endometriotic cells compared to endometrial cells. CRABP2 knockdown in endometrial cells increased survival, and FABP5 knockdown in endometriotic cells decreased survival without altering the expression of downstream nuclear retinoic acid receptor α and peroxisome-proliferator-activated receptor β/δ.
conclusionsIn endometrial stromal cells, progesterone receptor up-regulates expression of STRA6 and CRABP2, which control retinol uptake and growth-suppressor actions of RA. In endometriotic stromal cells, decreased expression of these genes leads to decreased retinol uptake and dominant FABP5-mediated prosurvival activity.
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.