ArticleAmerican journal of physiology. Cell physiology2012
ERK acts in parallel to PKCδ to mediate the connexin43-dependent potentiation of Runx2 activity by FGF2 in MC3T3 osteoblasts.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- Gap Junctions or Hemichannel-Dependent and Independent Roles of Connexins in Fibrosis, Epithelial-Mesenchymal Transitions, and Wound Healing.Biomolecules · 2023Review
- Connexin 43 Promotes Neurogenesis via Regulating Aquaporin-4 after Cerebral Ischemia.Neurotoxicity research · 2023Article
- Connexin43 in Musculoskeletal System: New Targets for Development and Disease Progression.Aging and disease · 2022Article
- Bone fracture healing: perspectives according to molecular basis.Journal of bone and mineral metabolism · 2021Review
- Relationship Between Hematoma Expansion Induced by Hypertension and Hyperglycemia and Blood-brain Barrier Disruption in Mice and Its Possible Mechanism: Role of Aquaporin-4 and Connexin43.Neuroscience bulletin · 2020Article
- Connexin43 regulates osteoprotegerin expression via ERK1/2 -dependent recruitment of Sp1.Biochemical and biophysical research communications · 2019Article
- Molecular signaling in bone cells: Regulation of cell differentiation and survival.Advances in protein chemistry and structural biology · 2019Review
- FGF-7 Dictates Osteocyte Cell Processes Through Beta-Catenin Transduction.Scientific reports · 2018Article
- Connexin43 and Runx2 Interact to Affect Cortical Bone Geometry, Skeletal Development, and Osteoblast and Osteoclast Function.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Defective signaling, osteoblastogenesis and bone remodeling in a mouse model of connexin 43 C-terminal truncation.Journal of cell science · 2017Article
- Connexin43 and the Intercellular Signaling Network Regulating Skeletal Remodeling.Current osteoporosis reports · 2017Review
- Novel multi-functional fluid flow device for studying cellular mechanotransduction.Journal of biomechanics · 2016Article
- Deficiency of the intermediate filament synemin reduces bone mass in vivo.American journal of physiology. Cell physiology · 2016Article
- Inhibition of connexin 43 prevents trauma-induced heterotopic ossification.Scientific reports · 2016Article
- Communication of cAMP by connexin43 gap junctions regulates osteoblast signaling and gene expression.Cellular signalling · 2016Article
- Connexins in the skeleton.Seminars in cell & developmental biology · 2016Review
- GnRH regulates trophoblast invasion via RUNX2-mediated MMP2/9 expression.Molecular human reproduction · 2016Article
- A cost-effective method to enhance adenoviral transduction of primary murine osteoblasts and bone marrow stromal cells.Bone research · 2016Article
- A Functional Assay to Assess Connexin 43-Mediated Cell-to-Cell Communication of Second Messengers in Cultured Bone Cells.Methods in molecular biology (Clifton, N.J.) · 2016Article
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6 authors at 1 institution in 1 country.
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Abstract
The gap junction protein, connexin43 (Cx43), plays an important role in skeletal biology. Previously, we have shown that Cx43 can enhance the signaling and transcriptional response to fibroblast growth factor 2 (FGF2) in osteoblasts by increasing protein kinase C-δ (PKCδ) activation to affect Runx2 activity. In the present study, we show by luciferase reporter assays that the ERK signaling cascade acts in parallel to PKCδ to modulate Runx2 activity downstream of the Cx43-dependent amplification of FGF2 signaling. The PKCδ-independent activation of ERK by FGF2 was confirmed by Western blotting, as was the Cx43-dependent enhancement of ERK activation. Consistent with our prior observations for PKCδ, flow cytometry analyses show that Cx43 overexpression enhances the percentage of phospho-ERK-positive cells in response to FGF2, supporting the notion that shared signals among gap junction-coupled cells result in the enhanced response to FGF2. Western blots and luciferase reporter assays performed on osteoblasts cultured under low-density and high-density conditions revealed that cell-cell contacts are required for Cx43 to amplify ERK activation and gene transcription. Similarly, inhibition of gap junctional communication with the channel blocker 18β-glycyrrhetinic acid attenuates the Cx43-dependent enhancement of Runx2-transcriptional activity. In total, these data underscore the importance of cell-cell communication and activation of the ERK and PKCδ pathways in the coordination of the osteoblast response to FGF2 among populations of osteoblasts.
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