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Interferon-gamma suppresses Na(+)-H(+) exchanger in cultured human endolymphatic sac epithelial cells

jiekel 添加于 2009-7-6 05:10 | 1756 次阅读 | 0 个评论
  •  作 者

    Son EJ, Moon IS, Kim SH, Kim SJ, Choi JY
  •  摘 要

    Adequate regulation of endolymphatic pH is essential for maintaining inner ear function. The Na(+)-H(+) exchanger (NHE) is a major determinant of intracellular pH (pH(i)), and facilitates Na(+) and fluid absorption in various epithelia. We determined the functional and molecular expression of NHEs in cultured human endolymphatic sac (ES) epithelial cells and examined the effect of IFN-gamma on NHE function. Serial cultures of human ES epithelial cells were generated from tissue samples. The molecular expression of NHE1, -2, and -3 isoforms was determined by real-time RT-PCR. The functional activity of NHE isoforms was measured microfluorometrically using a pH-sensitive fluorescent dye, 2',7'-bis(carbonylethyl)-5(6)-carboxyfluorescein (BCECF), and a NHE-inhibitor, 3-methylsulfonyl-4-piperidinobenzoyl guanidine methanesulfonate (HOE694). NHE1, -2, and -3 mRNAs were expressed in human ES epithelial cells. Functional activity of NHE1 and -2 was confirmed in the luminal membrane of ES epithelial cells by sequentially suppressing Na(+)-dependent pH(i) recovery from intracellular acidification using different concentrations of HOE694. Treatment with IFN-gamma (50 nM for 24 h) suppressed mRNA expression of NHE1 and -2. IFN-gamma also suppressed functional activity of both NHE1 and -2 in the luminal membrane of ES epithelial cells. This study shows that NHEs are expressed in cultured human ES epithelial cells and that treatment with IFN-gamma suppresses the expression and functional activity of NHE1 and -2. J. Cell. Biochem. (c) 2009 Wiley-Liss, Inc.
  •  详细资料

    • 文献种类:期刊
    • 期刊名称: Journal of Cellular Biochemistry
    • 期刊缩写: J Cell Biochem
    • 期卷页: 2009
    • 地址: Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, South Korea
    • ISBN: 1097-4644
    • 备注:PMID:19479940
  • 相关链接 DOI URL 

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