Oxygen-evoked Na+ transport in rat fetal distal lung epithelial cells
Oxygen-evoked Na+ transport in rat fetal distal lung epithelial cells
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DOI：
10.1111/j.1469-7793.2001.0105g.x
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发表时间：
2001-04-01
影响因子：
5.5
通讯作者：
Wilson, SM
中科院分区：
文献类型：
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作者：
Baines, DL;Ramminger, SJ;Wilson, SM
1. 大鼠胎儿远端肺上皮 (FDLE) 细胞的单层培养物在新生儿肺泡 P-O2 (100 mmHg) 维持 (48 小时) 时产生比胎儿 P-O2 (23 mmHg) 更大的自发短路电流 (I-SC)。当细胞在这些气氛之间转移以增加与出生时相同的 P-O2 时，6 小时后没有看到 I-SC 增加，但反应在 24 小时时完全建立。2。对基底外侧通透细胞的研究显示，P-O2 升高 6 小时后，顶端 Na+ 电导 (G(Na)) 略有上升，但到 24 小时，没有发生进一步的变化。然而，48 小时后出现大幅上升。3。报告基因检测显示，P-O2 升高后 24 小时，未观察到 α -ENaC（上皮 Naf 通道 α 亚基）启动子的激活，但在 48 小时时观察到转录活性增加。4。对顶部通透细胞的研究表明，P-O2 升高后 6 小时，Na+ 泵容量明显小幅上升，并且与 I-SC 的上升一样，这种效应在 24 小时时完全确立。因此，在 P-O2 升高后 6-24 小时，I-SC 会升高，这主要是由于 Na+ 泵容量的增加。5。因此，G(Na) 的增加与 α -ENaC 启动子的激活同时发生，但这些效应发生在 I-SC 的上升完全建立之后，因此不能成为这种生理反应的基础。转录增加可能是对 Na+ 转运增加的适应，而不是其原因。
1. Monolayer cultures of rat fetal distal lung epithelial (FDLE) cells generated larger spontaneous short circuit currents (I-SC) when maintained (48 h) at neonatal alveolar P-O2(100 mmHg) than at fetal P-O2 (23 mmHg). When cells were shifted between these atmospheres in order to impose a rise in P-O2 equivnlent to that seen at birth, no rise in I-SC was seen after 6 h but the response was fully established by 24 h.2. Studies of basolaterally permeabilised cells revealed a small rise in apical Na+ conductance (G(Na)) 6 h after P-O2 was raised but no further change had occurred by 24 h. A substantial rise was, however, seen after 48 h.3. Reporter gene assays showed that no activation of the alpha -ENaC (epithelial Naf channel alpha -subunit) promoter was discernible 24 h after P-O2 was raised but increased transcriptional activity was seen at 48 h.4. Studies of apically permeabilised cells showed that a small rise in Na+ pump capacity was evident 6 h after P-O2 was raised and, in common with the rise in I-SC, this effect was fully established by 24 h. The rise in I-SC thus develops 6-24 h after P-O2 is raised and is due, primarily, to increased Na+ pump capncity.5. The increase in G(Na) thus coincides with activation of the alpha -ENaC promoter but these effects occur after the rise in I-SC is fully established and so cannot underlie this physiological response. The increased transcription may he an adaptation to increased Na+ transport and not its cause.