Upregulation of Kv1.3 K(+) channels in microglia deactivated by TGF-beta.
Upregulation of Kv1.3 K(+) channels in microglia deactivated by TGF-beta.
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DOI：
10.1152/ajpcell.2000.279.4.c1123
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发表时间：
2000-10
期刊：
影响因子：
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通讯作者：
T. Schilling;Fred N. Quandt;V. Cherny;Wei Zhou;Uwe Heinemann;T. DeCoursey;Claudia Eder
中科院分区：
文献类型：
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作者：
T. Schilling;Fred N. Quandt;V. Cherny;Wei Zhou;Uwe Heinemann;T. DeCoursey;Claudia Eder
小胶质细胞活化伴随着K（+）通道表达的变化。在这里，我们证明了一个失活细胞因子改变小胶质细胞的电生理特性。在转化生长因子-β（TGF-β）作用24 h后，观察到小胶质细胞延迟整流（DR）K（+）通道的上调。相反，内向整流钾（+）通道的表达不受TGF-β的影响。DR电流密度在TGF-β处理的小胶质细胞中比未处理的小胶质细胞大六倍以上。TGF-β处理的细胞的DR电流表现出以下特性：在大于-40 mV的电位下激活，在-27 mV下半最大激活，在-38 mV下半最大失活，时间依赖性和强烈的使用依赖性失活，以及在林格溶液中13 pS的单通道电导。DR通道对卡里巴毒素（CTX）和钾毒素（KTX）高度敏感，而α-树毒素几乎没有影响。RT-PCR检测小胶质细胞中Kv1.3和Kir2.1的mRNA表达。根据观察到的DR电流密度的变化，Kv1.3的mRNA水平（通过竞争性RT-PCR评估）增加了五倍后，用TGF-β处理小胶质细胞。
Microglial activation is accompanied by changes in K(+) channel expression. Here we demonstrate that a deactivating cytokine changes the electrophysiological properties of microglial cells. Upregulation of delayed rectifier (DR) K(+) channels was observed in microglia after exposure to transforming growth factor-beta (TGF-beta) for 24 h. In contrast, inward rectifier K(+) channel expression was unchanged by TGF-beta. DR current density was more than sixfold larger in TGF-beta-treated microglia than in untreated microglia. DR currents of TGF-beta-treated cells exhibited the following properties: activation at potentials more positive than -40 mV, half-maximal activation at -27 mV, half-maximal inactivation at -38 mV, time dependent and strongly use-dependent inactivation, and a single channel conductance of 13 pS in Ringer solution. DR channels were highly sensitive to charybdotoxin (CTX) and kaliotoxin (KTX), whereas alpha-dendrotoxin had little effect. With RT-PCR, mRNA for Kv1.3 and Kir2.1 was detected in microglia. In accordance with the observed changes in DR current density, the mRNA level for Kv1.3 (assessed by competitive RT-PCR) increased fivefold after treatment of microglia with TGF-beta.