ArticlePloS one2011
Prostaglandin E2 signals through PTGER2 to regulate sclerostin expression.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 76 citations in OpenAlex.
- Spatial transcriptomics in bone mechanomics: Exploring the mechanoregulation of fracture healing in the era of spatial omics.Science advances · 2025Article
- Isolation, Purification, Generation, and Culture of Osteocytes.Methods in molecular biology (Clifton, N.J.) · 2025Article
- SOST/Sclerostin impairs the osteogenesis and angiogesis in glucocorticoid-associated osteonecrosis of femoral head.Molecular medicine (Cambridge, Mass.) · 2024Article
- Antisclerostin Effect on Osseointegration and Bone Remodeling.Journal of clinical medicine · 2023Review
- Paracrine and endocrine functions of osteocytes.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2023Review
- Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023Review
- Positive and Negative Regulators of Sclerostin Expression.International journal of molecular sciences · 2022Review
- Immune mechanism of low bone mineral density caused by ankylosing spondylitis based on bioinformatics and machine learning.Frontiers in genetics · 2022Article
- Osteocytes as main responders to low-intensity pulsed ultrasound treatment during fracture healing.Scientific reports · 2021Article
- Mechanical strain-mediated reduction in RANKL expression is associated with RUNX2 and BRD2.Gene: X · 2020Article
- Is There a Governing Role of Osteocytes in Bone Tissue Regeneration?Current osteoporosis reports · 2020Review
- Review
- The Role of Sclerostin in Bone and Ectopic Calcification.International journal of molecular sciences · 2020Review
- The Osteocyte: New Insights.Annual review of physiology · 2020Review
- Connexin43 enhances Wnt and PGE2-dependent activation of β-catenin in osteoblasts.Pflugers Archiv : European journal of physiology · 2019Article
- SOST, an LNGFR target, inhibits the osteogenic differentiation of rat ectomesenchymal stem cells.Cell proliferation · 2018Article
- Biological responses of osteocytic connexin 43 hemichannels to simulated microgravity.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- The role of adaptive bone formation in the etiology of stress fracture.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Sost, independent of the non-coding enhancer ECR5, is required for bone mechanoadaptation.Bone · 2016Article
- Communication of cAMP by connexin43 gap junctions regulates osteoblast signaling and gene expression.Cellular signalling · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Wnt signaling pathway is a robust regulator of skeletal homeostasis. Gain-of-function mutations promote high bone mass, whereas loss of Lrp5 or Lrp6 co-receptors decrease bone mass. Similarly, mutations in antagonists of Wnt signaling influence skeletal integrity, in an inverse relation to Lrp receptor mutations. Loss of the Wnt antagonist Sclerostin (Sost) produces the generalized skeletal hyperostotic condition of sclerosteosis, which is characterized by increased bone mass and density due to hyperactive osteoblast function. Here we demonstrate that prostaglandin E(2) (PGE(2)), a paracrine factor with pleiotropic effects on osteoblasts and osteoclasts, decreases Sclerostin expression in osteoblastic UMR106.01 cells. Decreased Sost expression correlates with increased expression of Wnt/TCF target genes Axin2 and Tcf3. We also show that the suppressive effect of PGE(2) is mediated through a cyclic AMP/PKA pathway. Furthermore, selective agonists for the PGE(2) receptor EP2 mimic the effect of PGE(2) upon Sost, and siRNA reduction in Ptger2 prevents PGE(2)-induced Sost repression. These results indicate a functional relationship between prostaglandins and the Wnt/β-catenin signaling pathway in bone.
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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.