کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5562202 1562607 2017 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Fascin2 regulates cisplatin-induced apoptosis in NRK-52E cells
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Fascin2 regulates cisplatin-induced apoptosis in NRK-52E cells
چکیده انگلیسی


- Cisplatin induces loss of fascin2 protein expression in vitro and in vivo.
- Fascin2 is regulated, in part, by α(E)-catenin.
- Knockdown of fascin2 increases susceptibility to cisplatin nephrotoxicity in vitro.
- Overexpression of fascin2 is renoprotective against cisplatin injury in vitro.

Previous studies have shown that the aging kidney has a marked loss of α(E)-catenin in proximal tubular epithelium. α-Catenin, a key regulator of the actin cytoskeleton, interacts with a variety of actin-binding proteins. Cisplatin-induced loss of fascin2, an actin bundling protein, was observed in cells with a stable knockdown of α(E)-catenin (C2 cells), as well as in aging (24 mon), but not young (4 mon), kidney. Fascin2 co-localized with α-catenin and the actin cytoskeleton in NRK-52E cells. Knockdown of fascin2 increased the susceptibility of tubular epithelial cells to cisplatin-induced injury. Overexpression of fascin2 in C2 cells restored actin stress fibers and attenuated the increased sensitivity of C2 cells to cisplatin-induced apoptosis. Interestingly, fascin2 overexpression attenuated cisplatin-induced mitochondrial dysfunction and oxidative stress in C2 cells. These data demonstrate that fascin2, a putative target of α(E)-catenin, may play important role in preventing cisplatin-induced acute kidney injury.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 266, 15 January 2017, Pages 56-64
نویسندگان
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