Phorbol ester and okadaic acid regulation of Na-2Cl-K cotransport in rabbit tracheal epithelial cells.
Phorbol ester and okadaic acid regulation of Na-2Cl-K cotransport in rabbit tracheal epithelial cells.
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佛波酯和冈田酸对兔气管上皮细胞中 Na-2Cl-K 共转运的调节。
DOI：
10.1152/ajpcell.1996.271.1.c338
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Thomas,L
中科院分区：
文献类型：
--
作者：
Liedtke,CM;Thomas,L
We evaluated a role for protein kinase C (PKC) in the regulation of rabbit tracheal epithelial Na-Cl(K) cotransport. Short-term treatment with phorbol 12-myristate 13-acetate (PMA) dose dependently increased bumetanide-sensitive Na and Cl efflux and elevated staurosporine- and bumetanide-sensitive Na, Cl, and K uptake. PMA and the alpha 2A-adrenergic agonist guanabenz both induced contransport with a stoichiometry of 2 Cl:1 Na and 2 Cl:1 Rb and elevated staurosporine-sensitive PKC activity in cytosolic and particulate fractions. Prolonged PMA treatment did not sustain bumetanide-sensitive 2 Cl:1 Na and 2 Cl:1 Rb transport but did block stimulation of bumetanide-sensitive transport by PMA or guanabenz and elevation of PKC activity by PMA and guanabenz in a particulate fraction. Cells treated with okadaic acid exhibited a staurosporine- and bumetanide-sensitive 2 Cl:1 Na and 2 Cl:1 Rb uptake. In cultured monolayers, basolateral perfusion with epinephrine, isoproterenol, or PMA increased short-circuit current (Isc). Basolateral application of bumetanide reduced elevated Isc to baseline levels, indicating a role for Cl secretory cells in a reconstituted tracheal epithelium. Pretreatment of transmonolayer cultures with PMA diminished the stimulatory response to epinephrine. These results indicate that, in rabbit tracheal epithelial cells, alpha-adrenergic stimulation activated Na-2Cl-K cotransport and that PKC is a critical effector in this process.
α2A 肾上腺素受体通过百日咳毒素敏感 G 蛋白激活人血小板中的蛋白激酶 C
影响因子：
3.5
作者：
Rienk Nieuwiand;O. Wijburg;G. van Willigen;J. Akkerman
通讯作者：
J. Akkerman