Pflügers Archiv

, Volume 447, Issue 3, pp 312–315

Effects of kinase inhibitors on TGF-β induced upregulation of Kv1.3 K+ channels in brain macrophages

Ion Channels, Transporters

DOI: 10.1007/s00424-003-1155-3

Cite this article as:
Schilling, T. & Eder, C. Pflugers Arch - Eur J Physiol (2003) 447: 312. doi:10.1007/s00424-003-1155-3


Deactivation of brain macrophages (microglia) by transforming growth factor-β (TGF-β) is characterized by enhanced Kv1.3 K+ channel expression. The intracellular mechanisms by which TGF-β causes K+ channel upregulation in microglia have remained unclear. We show here that the protein kinase inhibitor H7 abolishes TGF-β-induced increases in delayed rectifier K+ current density. However, this effect cannot be related to inhibition of protein kinase C (PKC) or protein kinase A (PKA) activity, because specific PKC and PKA inhibitors did not exhibit effects identical to H7. TGF-β-induced Kv1.3 channel expression was also unaffected by inhibitors of tyrosine kinase, Ca2+/calmodulin kinase II and mitogen-activated protein (MAP) kinase ERK. In contrast, delayed rectifier K+ current density was larger in TGF-β-stimulated cells pretreated with the p38 MAP kinase inhibitor SB203580 or the phosphatidylinositol 3-OH (PI3) kinase inhibitor wortmannin, suggesting that both p38 MAP kinase and PI3 kinase regulate negatively the upregulation of Kv1.3 K+ channels in TGF-β-treated microglial cells.


Brain macrophagesDelayed rectifier K+ currentH7p38 MAP kinasePI3 kinase

Copyright information

© Springer-Verlag  2003

Authors and Affiliations

  1. 1.Institut für Physiologie der CharitéHumboldt UniversitätBerlinGermany