Lipopolysaccharide changes the subcellular distribution of aquaporin 5 and increases plasma membrane water permeability in mouse lung epithelial cells
Lipopolysaccharide changes the subcellular distribution of aquaporin 5 and increases plasma membrane water permeability in mouse lung epithelial cells
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DOI：
10.1016/j.bbrc.2004.10.216
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发表时间：
2005-01-21
影响因子：
3.1
通讯作者：
Isohama, Y
中科院分区：
文献类型：
--
作者：
Ohinata, A;Nagai, K;Isohama, Y
水通道蛋白5（AQP 5）是肺上皮细胞的主要水通道，在维持肺内水平衡中起重要作用。AQP 5的细胞表面表达不仅受mRNA和蛋白质合成的调节，而且还受亚细胞分布的变化的调节。我们研究了脂多糖（LPS）对小鼠肺上皮细胞系（MLE-12）中AQP 5亚细胞分布的影响。LPS作用0.5 ~ 2 h后，细胞膜上AQP 5表达显著增加。免疫荧光和Western blotting强烈表明，LPS改变了AQP 5的亚细胞分布从细胞内囊泡室质膜。特异性p38 MAP激酶抑制剂SB 203580明显阻止LPS诱导的AQP 5分布变化。此外，LPS增加了MLE-12细胞的渗透水通透性。这些结果表明，LPS通过改变其亚细胞分布增加细胞表面AQP 5的表达，并通过激活p38 MAP激酶增加膜渗透水的通透性。(C)2004年爱思唯尔公司All rights reserved.
Aquaporin-5 (AQP5), a major water channel in lung epithelial cells, plays an important role in maintaining water homeostasis in the lungs. Cell surface expression of AQP5 is regulated by not only mRNA and protein synthesis but also changes in subcellular distribution. We investigated the effect of lipopolysaccharide (LPS) on the subcellular distribution of AQP5 in a mouse lung epithelial cell line (MLE-12). LPS caused significant increases in AQP5 in the plasma membrane at 0.5-2 h. Immunofluorescence and Western blotting strongly suggested that LPS altered AQP5 subcellular distribution from an intracellular vesicular compartment to the plasma membrane. The specific p38 MAP kinase inhibitor SB 203580 apparently prevented LPS-induced changes in AQP5 distribution. Furthermore, LPS increased the osmotic water permeability of MLE-12 cells. These findings demonstrate that LPS increases cell surface AQP5 expression by changing its subcellular distribution and increases membrane osmotic water permeability through activation of p38 MAP kinase. (C) 2004 Elsevier Inc. All rights reserved.