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Am J Physiol Cell Physiol 284: C85-C93, 2003; doi:10.1152/ajpcell.00145.2002
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Vol. 284, Issue 1, C85-C93, January 2003

PDGF upregulates delayed rectifier via Src family kinases and sphingosine kinase in oligodendroglial progenitors

Betty Soliven1, Lan Ma1, Hyun Bae1, Bernard Attali2, Alexander Sobko3, and Tamaki Iwase1

1 Department of Neurology and Committee on Neurobiology, The Brain Research Institute, University of Chicago, Chicago, Illinois 60637; 2 Department of Physiology, Sackler Medical School, Tel Aviv University, Ramat Aviv, 69978 Tel Aviv, Israel; and 3 Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093

An increase in the expression of the delayed rectifier current (IK) has been shown to correlate with mitogenesis in many cell types. However, pathways involved in the upregulation of IK by growth factors in oligodendroglial progenitors (OPs) have not been well-elucidated. In this study, we found that treatment with platelet-derived growth factor (PDGF) and basic fibroblast growth factor but not ciliary neurotrophic factor resulted in increased IK density and upregulation of Kv1.5 and Kv1.6 mRNA transcripts. The effect of PDGF on IK was blocked by mimosine, a cell cycle inhibitor, and by genistein, a tyrosine kinase inhibitor. Using inhibitors of PDGF-activated pathways, we found that PDGF-induced upregulation of Kv1.5 and IK density involves Src family tyrosine kinases, sphingosine kinase, and intracellular Ca2+ but not ERK1/2 or phosphatidylinositol 3-kinase pathways. Furthermore, agents that were effective inhibitors of PDGF-induced IK upregulation also attenuated OP proliferation, supporting the concept that IK is an important link between PDGF-activated signaling cascades and cell cycle progression.

ion channel modulation; Kv subunits; glia; oligodendrocyte progenitors; growth factors


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