MicroRNA 16 modulates epithelial sodium channel in human alveolar epithelial cells
نویسندگان
چکیده
منابع مشابه
Oxidized glutathione (GSSG) inhibits epithelial sodium channel activity in primary alveolar epithelial cells.
Amiloride-sensitive epithelial Na(+) channels (ENaC) regulate fluid balance in the alveoli and are regulated by oxidative stress. Since glutathione (GSH) is the predominant antioxidant in the lungs, we proposed that changes in glutathione redox potential (Eh) would alter cell signaling and have an effect on ENaC open probability (Po). In the present study, we used single channel patch-clamp rec...
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Electrolyte transport across the adult alveolar epithelium plays an important role in maintaining a thin fluid layer along the apical surface of the alveolus that facilitates gas exchange across the epithelium. Most of the work published on the transport properties of alveolar epithelial cells has focused on the mechanisms and regulation of Na(+) transport and, in particular, the role of amilor...
متن کاملEpithelial cells, Exracellular matrix
چکیده مقدمه: ماده خارج سلولی به عنوان بخش مهم ریز محیطMicroenvironment)(، نقش اساسی در نگهداری وضعیت تمایز دارد. در بررسی‌های گذشته، این اثر در برخی سلول‌ها از جمله سلول‌های پوششی لوله رحم و یا رحم مطالعه شده است. در این پژوهش‌ها، برای حفظ تمایز سلول ، علاوه بر ماده خارج سلولی عوامل دیگر‌ی مانند هورمون‌ها، فاکتورهای رشد و سلول‌های داربستی نیز بکار رفته است ولی فر...
متن کاملHypoxia downregulates expression and activity of epithelial sodium channels in rat alveolar epithelial cells.
Decrease in alveolar oxygen tension may induce acute lung injury with pulmonary edema. We investigated whether, in alveolar epithelial cells, expression and activity of epithelial sodium (Na) channels and Na,K-adenosine triphosphatase, the major components of transepithelial Na transport, were regulated by hypoxia. Exposure of cultured rat alveolar cells to 3% and 0% O2 for 18 h reduced Na chan...
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ژورنال
عنوان ژورنال: Biochemical and Biophysical Research Communications
سال: 2012
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2012.08.063