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TRB3通过调节Akt-PKB通路介导白蛋白超负荷诱导的近端肾小管细胞凋亡.doc

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TRB3通过调节Akt-PKB通路介导白蛋白超负荷诱导的近端肾小管细胞凋亡.doc

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TRB3通过调节Akt-PKB通路介导白蛋白超负荷诱导的近端肾小管细胞凋亡.doc

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TRB3 mediates apoptosis of renal proximal tubular cells
induced by albumin-overload through Akt/PKB pathway#
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Wang Weiwei1, Liu Gang2, Lv Shasha1, Cheng Jing2, Liu Xiangchun1, Liu Haiying2,
Guan Guangju2**
(1. Medical School, Shandong University, Jinan 250012;
2. Department of Nephrology, the Second Hospital of Shandong University, Jinan 250033)
Abstract: Albuminuria contributes to the development of chronic kidney disease (CKD), but the
mechanisms are not fully understood. TRB3 is a kinase-like molecule that modifies cellular survival
and metabolism and interferes with signal transduction pathways. We sought to determine whether
TRB3 participates in apoptosis of renal proximal tubular cells stimulated by albumin overload.
NRK-52E cells, a rat proximal tubular cell line, were incubated with various concentrations of fatty
acid and endotoxin-free bovine serum albumin(BSA) for a variety of durations. Quantitative real-time
PCR and western blot were used to determine TRB3 mRNA and protein expression separately.
Apoptosis was detected by ssDNA ELISA assay and caspase3 activity measurement. Then gene
silencing was used to investigate whether TRB3 participated in apoptosis of NRK-52E cells induced by
BSA and through what signaling pathway it works. We found that BSA induced apoptosis in a time-
and dose-dependent manner in NRK-52E