ArticleThe Biochemical journal2003
Extracellular ATP stimulates the early growth response protein 1 (Egr-1) via a protein kinase C-dependent pathway in the human osteoblastic HOBIT cell line.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- Extracellular ATP and its derivatives provide spatiotemporal guidance for bone adaptation to wide spectrum of physical forces.Bone reports · 2022Review
- Purinergic Signaling Mediates PTH and Fluid Flow-Induced Osteoblast Proliferation.BioMed research international · 2021Article
- Mechanically stimulated ATP release from murine bone cells is regulated by a balance of injury and repair.eLife · 2018Article
- Paradoxical induction of growth arrest and apoptosis by EGF via the up-regulation of PTEN by activating Redox factor-1/Egr-1 in human lung cancer cells.Oncotarget · 2017Article
- P2Y2 purinergic receptor activation is essential for efficient hepatocyte proliferation in response to partial hepatectomy.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Purinergic signalling in the musculoskeletal system.Purinergic signalling · 2013Review
- Dose-dependent differential effects of risedronate on gene expression in osteoblasts.Biochemical pharmacology · 2011Article
- Gap Junctions and Biophysical Regulation of Bone Cells.Clinical reviews in bone and mineral metabolism · 2010Article
- Functional characterization of genetic variation in the Frizzled 1 (FZD1) promoter and association with bone phenotypes: more to the LRP5 story?Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2009Article
- P2X7 receptors on osteoblasts couple to production of lysophosphatidic acid: a signaling axis promoting osteogenesis.The Journal of cell biology · 2008Article
- Mechanotransduction in human bone: in vitro cellular physiology that underpins bone changes with exercise.Sports medicine (Auckland, N.Z.) · 2008Review
- Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks.Purinergic signalling · 2006Article
- Activation of APE1/Ref-1 is dependent on reactive oxygen species generated after purinergic receptor stimulation by ATP.Nucleic acids research · 2005Article
- Expression of P2Y nucleotide receptors and ectonucleotidases in quiescent and activated rat hepatic stellate cells.American journal of physiology. Gastrointestinal and liver physiology · 2004Article
- Agonist-dependence of recovery from desensitization of P2X(3) receptors provides a novel and sensitive approach for their rapid up or downregulation.British journal of pharmacology · 2004Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular nucleotides exert an important role in controlling cell physiology by activating intracellular signalling cascades. Osteoblast HOBIT cells express P2Y(1) and P2Y(2) G-protein-coupled receptors, and respond to extracellular ATP by increasing cytosolic calcium concentrations. Early growth response protein 1 (Egr-1) is a C(2)H(2)-zinc-finger-containing transcriptional regulator responsible for the activation of several genes involved in the control of cell proliferation and apoptosis, and is thought to have a central role in osteoblast biology. We show that ATP treatment of HOBIT cells increases Egr-1 protein levels and binding activity via a mechanism involving a Ca(2+)-independent protein kinase C isoform. Moreover, hypotonic stress and increased medium turbulence, by inducing ATP release, result in a similar effect on Egr-1. Increased levels of Egr-1 protein expression and activity are achieved at very early times after stimulation (5 min), possibly accounting for a rapid way for changing the osteoblast gene-expression profile. A target gene for Egr-1 that is fundamental in osteoblast physiology, COL1A2, is up-regulated by ATP stimulation of HOBIT cells in a timescale that is compatible with that of Egr-1 activation.
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