Hormones increase mRNA of cyclic-nucleotide-gated cation channels in airway epithelia.

Hormones increase mRNA of cyclic-nucleotide-gated cation channels in airway epithelia.
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激素增加气道上皮细胞中环核苷酸门控阳离子通道的 mRNA。

DOI:
10.1007/s004240000359
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发表时间:
2000
期刊:
Pflugers Archiv : European journal of physiology.
影响因子:
--
通讯作者:
Guggino,SE
Guggino,SE
中科院分区:
--
文献类型:
--
作者:
Qiu,W;Laheri,A;Leung,S;Guggino,SE

文献摘要

相似文献

Previous studies have shown that the mRNA of cyclic-nucleotide-gated nonselective cation (CNG) channels is expressed in rat airway epithelia and that these channels contribute to sodium-mediated short-circuit currents in cultured rat tracheal epithelia. Patch-clamp studies from human A549 cells indicate that these channels contribute to cGMP-stimulatedl-cis-diltiazem- and dichlorobenzamil-inhibited whole-cell sodium currents. This study demonstrates that mRNA for primary and secondary subunits of CNG channels, hαCNG1 and hβCNG1 respectively, are expressed in several human airway cell lines, including normal and cystic fibrosis bronchial airway cells, in normal and cystic fibrosis tracheal airway cell lines and nasal polyp tissue from a cystic fibrosis patient. The mRNA of rαCNG1 in rat lung increased in response to increased circulating glucocorticoids and decreased in animals with lowered circulating glucocorticoids after aminoglutethimide treatment. Likewise the mRNA of hαCNG1 increased in the presence of glucocorticoids in cultured alveolar airway cells. The mRNA of αCNG1 in rat lung was also increased in response to a low-salt diet and lowered in animals fed a high-salt diet. Likewise the mRNA of αCNG1 was increased in response to increased aldosterone and decreased in animals given spironolactone. These results suggest that mRNA for αCNG1 increases in response to elevated glucocorticoids or mineralocorticoids. Because αCNG1 is a functional sodium entry channel in both rat and human airway epithelial cells, if channel protein is also elevated this channel could mediate an increase in sodium absorption across lung epithelia in response to circulating hormones.