| Autor: |
Soliven, Betty, Lan Ma, Hyun Bae, Attali, Bernard, Sobko, Alexander, Iwase, Tamaki |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Cell Physiology; Jan2003, Vol. 284 Issue 1, pC85, 9p, 4 Black and White Photographs, 13 Graphs |
| Abstrakt: |
An increase in the expression of the delayed rectifier current (I[sub K]) has been shown to correlate with mitogenesis in many cell types. However, pathways involved in the upregulation of I[sub K] 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 I[sub K] density and upregulation of Kv1.5 and Kv1.6 mRNA transcripts. The effect of PDGF on I[sub K] 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 I[sub K] density involves Src family tyrosine kinases, sphingosine kinase, and intracellular Ca[sup 2+] but not ERK½ or phosphatidylinositol 3-kinase pathways. Furthermore, agents that were effective inhibitors of PDGFinduced I[sub K] upregulation also attenuated OP proliferation, supporting the concept that I[sub K] is an important link between PDGF-activated signaling cascades and cell cycle progression. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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