ArticleReproductive biology and endocrinology : RB&E2003
Gonadotropin releasing hormone analogue (GnRHa) alters the expression and activation of Smad in human endometrial epithelial and stromal cells.
Article in Reproductive biology and endocrinology : RB&E, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
What it found
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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.
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
8 citing papers in PubMed, 23 citations in OpenAlex.
- The impact of long-acting Gonadotropin-releasing hormone agonist pretreatment on the clinical pregnancy outcomes of hormone replacement therapy-frozen embryo transfer in recurrent implantation failure patients with and without polycystic ovary syndrome: a retrospective clinical study.BMC pregnancy and childbirth · 2025Article
- Article
- Noncanonical functions of glucocorticoids: A novel role for glucocorticoids in performing multiple beneficial functions in endometrial stem cells.Cell death & disease · 2021Article
- Retraction Note to: Gonadotropin releasing hormone analogue (GnRHa) alters the expression and activation of Smad in human endometrial epithelial and stromal cells.Reproductive biology and endocrinology : RB&E · 2015Article
- Liarozole inhibits transforming growth factor-β3--mediated extracellular matrix formation in human three-dimensional leiomyoma cultures.Fertility and sterility · 2014Article
- DNA profiling analysis of endometrial and ovarian cell lines reveals misidentification, redundancy and contamination.Gynecologic oncology · 2012Article
- Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta.Molecular human reproduction · 2009Article
- Association of common genetic variants in SMAD7 and risk of colon cancer.Carcinogenesis · 2009Article
Corrections and comments
- Retraction · 2015-04-03Falsification/Fabrication of Data · Investigation by ORI · · Nasser Chegini has finding of misconduct: https://ori.hhs.gov/content/case-summary-chegini-nasser
- Commented on by
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Gonadotropin releasing hormone analogues (GnRHa) are often used to regress endometriosis implants and prevent premature luteinizing hormone surges in women undergoing controlled ovarian stimulation. In addition to GnRH central action, the expression of GnRH and receptors in the endometrium implies an autocrine/paracrine role for GnRH and an additional site of action for GnRHa. To further examine the direct action of GnRH (Leuprolide acetate) in the endometrium, we determined the effect of GnRH on endometrial stromal (ESC) and endometrial surface epithelial (HES) cells expression and activation of Smads (Smad3, -4 and -7), intracellular signals activated by transforming growth factor beta (TGF-beta), a key cytokine expressed in the endometrium. The results show that GnRH (0.1 microM) increased the expression of inhibitory Smad7 mRNA in HES with a limited effect on ESC, while moderately increasing the common Smad4 and Smad7 protein levels in these cells (P < 0.05). GnRH in a dose--(0.01 to 10 microM) and time--(5 to 30 min) dependent manner decreased the rate of Smad3 activation (phospho-Smad3, pSmad3), and altered Smad3 cellular distribution in both cell types. Pretreatment with Antide (GnRH antagonist) resulted in further suppression of Smad3 induced by GnRH, with Antide inhibition of pSmad3 in ESC. Furthermore, co-treatment of the cells with GnRH + TGF-beta, or pretreatment with TGF-beta type II receptor antisense to block TGF-beta autocrine/paracrine action, in part inhibited TGF-beta activated Smad3. In conclusion, the results indicate that GnRH acts directly on the endometrial cells altering the expression and activation of Smads, a mechanism that could lead to interruption of TGF-beta receptor signaling mediated through this pathway in the endometrium.
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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.