ArticleThe Journal of physiology1993
Mitogenic factors regulate ion channels in Schwann cells cultured from newborn rat sciatic nerve.
Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 74 citations in OpenAlex.
- Plasmolipin and Its Role in Cell Processes.Molecular biology · 2021Article
- Bioelectric Properties of Myogenic Progenitor Cells.Bioelectricity · 2019Review
- Tonic ATP-mediated growth suppression in peripheral nerve glia requires arrestin-PP2 and is evaded in NF1.Acta neuropathologica communications · 2018Article
- Potassium channels in cell cycle and cell proliferation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- CFTR-deficient pigs display peripheral nervous system defects at birth.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Membrane potential and cancer progression.Frontiers in physiology · 2013Article
- Neuronal activity in the hub of extrasynaptic Schwann cell-axon interactions.Frontiers in cellular neuroscience · 2013Article
- Bioelectric controls of cell proliferation: ion channels, membrane voltage and the cell cycle.Cell cycle (Georgetown, Tex.) · 2009Review
- Involvement of chloride channels in IGF-I-induced proliferation of porcine arterial smooth muscle cells.Cardiovascular research · 2007Article
- A voltage-driven switch for ion-independent signaling by ether-à-go-go K+ channels.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Ca2+ signaling, intracellular pH and cell volume in cell proliferation.The Journal of membrane biology · 2005Review
- Mechanisms and roles of axon-Schwann cell interactions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Review
- The influence of cell volume changes on tumour cell proliferation.European biophysics journal : EBJ · 2004Review
- Expression of voltage-gated chloride channels in human glioma cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Gene-targeted deletion of neurofibromin enhances the expression of a transient outward K+ current in Schwann cells: a protein kinase A-mediated mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Volume-activated chloride currents contribute to the resting conductance and invasive migration of human glioma cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- The nuclear chloride ion channel NCC27 is involved in regulation of the cell cycle.The Journal of physiology · 2000Article
- Differential expression of volume-regulated anion channels during cell cycle progression of human cervical cancer cells.The Journal of physiology · 2000Article
- Heteromultimeric delayed-rectifier K+ channels in schwann cells: developmental expression and role in cell proliferation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Functional gap junctions in the schwann cell myelin sheath.The Journal of cell biology · 1998Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
1. Patch clamp studies were carried out in Schwann cells cultured from newborn rat sciatic nerve to determine the effects of mitogens on voltage-gated currents without the confounding influences of axonal contact and myelin present in vivo. The relevance of the various Schwann cell currents to proliferation was assessed using assays of [3H]thymidine incorporation. 2. Treatment of cultured Schwann cells with known mitogens, namely axon fragments (AF), myelin fragments (MF), or glial growth factor in combination with forskolin (GGF+F), increased the magnitudes of delayed rectifying potassium (K+) and sodium (Na+) currents. 3. In both control and mitogen-treated cells, the magnitude of net outward current paralleled clearly the magnitude of the cells' proliferative response. 4. The K+ channel-blocking quaternary ammonium ions, tetrabutylammonium (TBuA), tetrapentylammonium (TPeA) and tetrahexylammonium (THeA), but not the Na+ channel blocker tetrodotoxin (TTX), reduced proliferation in a dose-dependent fashion offering further evidence for a role for K+ channels in Schwann cell proliferation. 5. Voltage-gated chloride (Cl-) currents were observed in both control and mitogen-treated cells. Addition of the Cl- channel blockers, 4-acetamido-4'-isocyanatostilbene-2,2'-disulphonate (SITS) or 4,4'-diisothiocyanatostilbene-2,2'-disulphonate (DIDS), to the culture media enhanced proliferation. 6. The possible intermediary role of the Schwann cell resting potential was explored in ion substitution experiments by increasing the K+ concentration of the media and by adding ouabain. Both manipulations inhibited Schwann cell mitosis. 7. Comparison of the expression of functional ion channels in vitro with that previously described for Schwann cells in vivo suggests a difference in the Schwann cell response to the membrane fragment mitogens and their intact counterparts in regard to the regulation of ion channels. MF up-regulates the number of functional channels, whereas the elaboration of myelin (or a factor related to its presence) in vivo appears to down-regulate channel expression, at the cell soma of myelinating Schwann cells. In addition, axonal contact may be required for normal expression of functional inwardly rectifying K+ channels.
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