کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1938107 | 1050732 | 2007 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of p38 MAPK in hypotonic stress-induced stimulation of β- and γ-ENaC expression in renal epithelium
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We investigated a role of p38 MAPK in the regulation of transepithelial Na+ reabsorption by chronic application (20-24 h) of hypotonicity (hypotonic stress) in renal epithelial A6 cells. Pretreatment with a specific p38 MAPK inhibitor (SB202190) significantly reduced the chronic hypotonicity-stimulated transepithelial Na+ reabsorption by diminishing the Na+ entry through epithelial Na+ channel (ENaC) in the apical membrane and the Na+ extrusion via the Na+/K+ ATPase (pump), although the rate limiting step was still the Na+ entry step. We further examined whether the inhibitory effects of SB202190 on the transepithelial Na+ reabsorption is caused through suppression of mRNA expression of ENaC participating in the transepithelial Na+ reabsorption as the Na+ entry pathway. The chronic hypotonicity increased the mRNA expression of α-, β-, and γ-subunits of ENaC. Moreover, we found that inhibition of p38 MAPK by SB202190 diminished the mRNA expression of β- and γ-ENaC but not α-ENaC. Based on these observations, it is suggested that the chronic hypotonicity stimulates the renal transepithelial Na+ reabsorption by upregulating the mRNA expression of β- and γ-ENaC via a p38 MAPK-dependent pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 358, Issue 3, 6 July 2007, Pages 819-824
Journal: Biochemical and Biophysical Research Communications - Volume 358, Issue 3, 6 July 2007, Pages 819-824
نویسندگان
Naomi Niisato, Akiyuki Taruno, Yoshinori Marunaka,