کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8296804 | 1536770 | 2015 | 21 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CD36 is involved in high glucose-induced epithelial to mesenchymal transition in renal tubular epithelial cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: CD36 is involved in high glucose-induced epithelial to mesenchymal transition in renal tubular epithelial cells CD36 is involved in high glucose-induced epithelial to mesenchymal transition in renal tubular epithelial cells](/preview/png/8296804.png)
چکیده انگلیسی
The epithelial-to-mesenchymal transition (EMT) plays an important role in the progression of diabetic nephropathy. Our recent study showed that ROS mediated high glucose (HG)-induced EMT in renal tubular epithelial cells. CD36, a class-B scavenger receptor, has been reported to mediate the production of ROS in chronic kidney disease. In the present study, we examined the effect of inhibition of CD36 with CD36 siRNA or sulfosuccinimidyl-oleate (SSO), a CD36 antagonist, on HG-induced EMT in HK-2 cells. HG induced CD36 expression in a time-dependent manner in HK-2 cells. HG was shown to induce EMT at 72 h. This was blocked by knockdown of CD36 or treatment with SSO. Meanwhile, we also found that knockdown of CD36 or treatment with SSO inhibited HG-induced ROS generation, activation of ERK1/2 and Smad2, expression of TGF-β1 and synthesis of fibronectin. These data suggest that inhibition of CD36 prevented HG-induced EMT in HK-2 cells, highlighting CD36 as a potential therapeutic target for diabetic nephropathy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 468, Issues 1â2, 4â11 December 2015, Pages 281-286
Journal: Biochemical and Biophysical Research Communications - Volume 468, Issues 1â2, 4â11 December 2015, Pages 281-286
نویسندگان
Yanjuan Hou, Ming Wu, Jinying Wei, Yunzhuo Ren, Chunyang Du, Haijiang Wu, Ying Li, Yonghong Shi,