ArticleThe Journal of clinical endocrinology and metabolism2003
Differential expression, regulation, and induction of Smads, transforming growth factor-beta signal transduction pathway in leiomyoma, and myometrial smooth muscle cells and alteration by gonadotropin-releasing hormone analog.
Article in The Journal of clinical endocrinology and metabolism, 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 It has been retracted, and should not be counted.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 10 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.
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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.
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Who cites it
10 citing papers in PubMed, 46 citations in OpenAlex.
- Human Chorionic Gonadotrophin as a Possible Mediator of Leiomyoma Growth during Pregnancy: Molecular Mechanisms.International journal of molecular sciences · 2017Review
- Racial and ethnic differences in the pathogenesis and clinical manifestations of uterine leiomyoma.Seminars in reproductive medicine · 2013Article
- Gonadotropin-releasing hormone agonist increases expression of osmotic response genes in leiomyoma cells.Fertility and sterility · 2011Article
- Activation of the transforming growth factor beta pathway in bacterial otitis media.The Annals of otology, rhinology, and laryngology · 2011Article
- Human uterine leiomyoma-derived fibroblasts stimulate uterine leiomyoma cell proliferation and collagen type I production, and activate RTKs and TGF beta receptor signaling in coculture.Cell communication and signaling : CCS · 2010Article
- Proinflammatory and profibrotic mediators: principal effectors of leiomyoma development as a fibrotic disorder.Seminars in reproductive medicine · 2010Review
- Transforming growth factor beta3 regulates the versican variants in the extracellular matrix-rich uterine leiomyomas.Reproductive sciences (Thousand Oaks, Calif.) · 2009Article
- Genomic and proteomic profiling I: leiomyomas in African Americans and Caucasians.Reproductive biology and endocrinology : RB&E · 2007Article
- 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 · 2003Article
- Growth factors and myometrium: biological effects in uterine fibroid and possible clinical implications.Human reproduction updateReview
Corrections and comments
- Retraction · 2015-01-01Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Miscommunication with/by Author · · Nasser Chegini has finding of misconduct: https://ori.hhs.gov/content/case-summary-chegini-nasser
- Commented on by
- RetractedRetractions.2015
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The objective of this study was to further elucidate the role of TGFbeta and GnRH analog (GnRHa) in leiomyoma growth and regression. We examined the expression of Smads, TGFbeta receptor intracellular signaling molecules, in leiomyoma and myometrial smooth muscle cells (LSMC and MSMC), and determined whether TGFbeta and GnRHa differentially regulate their expression and induction in these cells. Using semiquantitative RT-PCR, Western blot analysis, and immunohistochemistry, we demonstrated that leiomyoma, myometrium, LSMC, and MSMC express receptor-activated Smad3, common Smad4, and the inhibitory Smad7 mRNA and protein and showed that TGFbeta1, in a time-dependent manner, transiently induced Smad7 expression, with Smad3 and Smad4 remaining largely unchanged. TGFbeta1 increased the rate of Smad and phosphorylated Smad3 (pSmad3) induction in both cell types. Pretreatment with TGFbeta type II receptor antisense oligonucleotide resulted in a trend toward a lower TGFbeta-induced pSmad3. GnRHa, in a dose- and time-dependent manner, increased the expression of Smad7 mRNA and the rapid induction of Smad3, Smad4, and Smad7 as well as pSmad3, which declined to control values at doses above 1 micro M in MSMC, but not in LSMC. GnRHa-induced pSamd3 was partly inhibited by a GnRH antagonist (antide). We concluded that leiomyoma, myometrium, LSMC, and MSMC express Smads, which are differentially expressed, induced, and activated by TGFbeta and are altered as a result of GnRHa treatment. These results suggest that TGFbeta and GnRHa mediate their actions through cross-talk involving Smads and most likely other signaling pathways that result in leiomyoma growth and regression.
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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.