ArticleJournal of bone metabolism2013
Bone Morphogenetic Protein-2 Desensitizes MC3T3-E1 Osteoblastic Cells to Estrogen Through Transcriptional Downregulation of Estrogen Receptor 1.
Article in Journal of bone metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Bazedoxifene and Beyond: Identifying This SERM's Targets and Deciphering Its Molecular Mechanisms.Advances in pharmacological and pharmaceutical sciences · 2026Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEstrogens exert preferable effects on bone metabolism through two estrogen receptors (ERs), ER1 and ER2, which activate the transcription of a set of genes as ligand-dependent transcription factors. Thus, growth factors and hormones which modulate ER expression in the bone, if any, may possibly modulate the effect of estrogens on bone metabolism. However, research as to which of these molecules regulate the expression of ERs in osteoblasts has not been well documented.
methodsA reporter assay system developed in this study was used to explore molecules that modulate ER1 expression in MC3T3-E1 osteoblastic cells. Gene expression was analyzed by reverse transcription-polymerase chain reaction.
resultsA pilot study using the reporter system revealed that bone morphogenetic protein (BMP)-2 negatively regulated ER1, but not ER2, expression in MC3T3-E1 cells. Consistently, estradiol-induced reporter activity via an estrogen responsive element was strongly suppressed in MC3T3-E1 cells pretreated with BMP-2.
conclusionsBMP-2 desensitizes osteoblastic cells to estrogen through downregulation of ER1 expression.
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Registered trials
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