PKC signaling in CF/T43 cell line: regulation of NKCC1 by PKC-delta isotype.
PKC signaling in CF/T43 cell line: regulation of NKCC1 by PKC-delta isotype.
复制标题
CF/T43 细胞系中的 PKC 信号传导：PKC-delta 同种型对 NKCC1 的调节。
DOI：
10.1016/s0167-4889(99)00146-9
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Cole,TS
中科院分区：
文献类型：
--
作者：
Liedtke,CM;Cole,TS
Cystic fibrosis (CF) airway epithelial cells have a reduced mass of ether-linked diacylglycerols which might alter protein kinase C (PKC)-regulated Cl secretion. PKC regulation of basolateral Na-K-2Cl cotransport (NKCC1) was investigated in CF nasal polyp epithelial cells and a CF/T43 cell line to ascertain whether PKC signaling was altered in CF. NKCC1 was detected as bumetanide-sensitive86Rb influx. Methoxamine, a α1-adrenergic agonist, increased PKC activity in cytosol and a particulate fraction for a prolonged time period, as predicted from previous studies on the generation of diglycerides induced with methoxamine. Short-term stimulation of CF/T43 cells for 40 s promoted a shift in PKC-δ and -ζ to a particulate fraction, increased activity of immune complexes of cytosolic PKC-δ and of particulate PKC-ζ and increased activity of NKCC1. Pretreatment with antisense oligonucleotide to PKC-δ blocked methoxamine-stimulated PKC-δ activity, reduced PKC-δ mass by 61.4%, and prevented methoxamine-stimulated activity of NKCC1. Sense and missense oligonucleotide to PKC-δ and antisense oligonucleotide to PKC-ζ did not alter expression of PKC-δ or the effects of methoxamine. These results demonstrate that PKC-δ-dependent activation of NKCC1 is preserved in CF cells and suggest that regulation of NKCC1 is independent of low ether-linked diglyceride mass.
