ArticleExperimental cell research2011
Purinergic signaling is required for fluid shear stress-induced NF-κB translocation in osteoblasts.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Differential contribution of THIK-1 KJournal of neuroinflammation · 2024Article
- The Impact of Plasma Membrane Ion Channels on Bone Remodeling in Response to Mechanical Stress, Oxidative Imbalance, and Acidosis.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Purinergic P2X7 Receptor Mediates the Elimination of Trichinella spiralis by Activating NF-κB/NLRP3/IL-1β Pathway in Macrophages.Infection and immunity · 2021Article
- The P2XFrontiers in cellular neuroscience · 2021Article
- P2X7 Interactions and Signaling - Making Head or Tail of It.Frontiers in molecular neuroscience · 2019Review
- Caveolin-1 regulates P2X7 receptor signaling in osteoblasts.American journal of physiology. Cell physiology · 2015Article
- [Genome-wide research on fluid shear stress-sensitive signaling pathways in MC3T3-E1 cells].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2014Article
- Hydraulic Pressure during Fluid Flow Regulates Purinergic Signaling and Cytoskeleton Organization of Osteoblasts.Cellular and molecular bioengineering · 2014Article
- The P2X7 receptor: a key player in immune-mediated bone loss?TheScientificWorldJournal · 2014Review
- Purinergic signalling in the musculoskeletal system.Purinergic signalling · 2013Review
- Suramin: a potential therapy for diabetic nephropathy.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Fluid shear stress regulates gene expression in osteoblasts, in part by activation of the transcription factor NF-κB. We examined whether this process was under the control of purinoceptor activation. MC3T3-E1 osteoblasts under static conditions expressed the NF-κB inhibitory protein IκBα and exhibited cytosolic localization of NF-κB. Under fluid shear stress, IκBα levels decreased, and concomitant nuclear localization of NF-κB was observed. Cells exposed to fluid shear stress in ATP-depleted medium exhibited no significant reduction in IκBα, and NF-κB remained within the cytosol. Similar results were found using oxidized ATP or Brilliant Blue G, P2X(7) receptor antagonists, indicating that the P2X(7) receptor is responsible for fluid shear-stress-induced IκBα degradation and nuclear accumulation of NF-κB. Pharmacologic blockage of the P2Y6 receptor also prevented shear-induced IκBα degradation. These phenomena involved neither ERK1/2 signaling nor autocrine activation by P2X(7)-generated lysophosphatidic acid. Our results suggest that fluid shear stress regulates NF-κB activity through the P2Y(6) and P2X(7) receptor.
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