ArticleThe Journal of clinical endocrinology and metabolism2003
The expression of Smads in human endometrium and regulation and induction in endometrial epithelial and stromal cells by transforming growth factor-beta.
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 It has been retracted, and should not be counted.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
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
10 citing papers in PubMed, 45 citations in OpenAlex.
- Endometriosis as an immune-mediated disease: pathogenetic mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- A functional role of LEFTY during progesterone therapy for endometrial carcinoma.Cell communication and signaling : CCS · 2017Article
- Activin A Stimulates Aromatase via the ALK4-Smad Pathway in Endometriosis.BioMed research international · 2016Article
- Expression of Nodal, Cripto, SMAD3, phosphorylated SMAD3, and SMAD4 in the proliferative endometrium of women with endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2015Article
- DNA profiling analysis of endometrial and ovarian cell lines reveals misidentification, redundancy and contamination.Gynecologic oncology · 2012Article
- miRNA signature and Dicer requirement during human endometrial stromal decidualization in vitro.PloS one · 2012Article
- Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta.Molecular human reproduction · 2009Article
- Androstenedione up-regulation of endometrial aromatase expression via local conversion to estrogen: potential relevance to the pathogenesis of endometriosis.The Journal of clinical endocrinology and metabolism · 2008Article
- Molecular profiling of experimental endometriosis identified gene expression patterns in common with human disease.Fertility and sterility · 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
Corrections and comments
- Retraction · 2015-01-01Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by ORI · Misconduct 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
Human endometrium expresses TGF-beta and TGF-beta receptors where they regulate several endometrial biological activities implicated in embryo implantation, irregular bleeding, endometriosis, and cancer. In the present study, we determined the expression of Smads, intracellular signals that mediate TGF-beta receptors signals from the cell surface to the nucleus, in the endometrium as well as isolated endometrial epithelial (EEC) and stromal (ESC) cells. We also determined whether TGF-beta regulates the expression Smads and activates Smad3 in these cells and endometrial surface epithelial cell line (HES). Using semiquantitative RT-PCR, Western blot analysis, and immunohistochemistry, we found that endometrium, EEC, ESC, and HES express Smad3, -4, and -7 mRNA and protein and contain phosphorylated Smad3 (pSmad3). Smads and pSmad3 were localized in the epithelial and stromal cells with cytoplasmic/nuclear localization. TGF-beta in a dose- and time-dependent manner increased the expression of Smads mRNA and protein, the rate of pSmad3 activation, and Smad3 translocation into the nucleus in ESC and HES. The effect of TGF-beta on pSmad3 induction was, in part, abrogated by the pretreatment of HES and ESC with TGF-beta type II receptor antisense oligonucleotides. We conclude that human endometrium expresses the necessary components of Smad signaling pathway, whose expression and induction in endometrial epithelial and stromal cells are regulated by TGF-beta.
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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.