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|標題:||Effect of aristolochic acid on intracellular calcium concentration and its links with apoptosis in renal tubular cells||作者:||Hsin, Y.H.
|關鍵字:||aristolochic acid;apoptosis;calcium;ER stress;GRP78;kidney;mitochondrial permeability transition;chinese herbs nephropathy;unfolded protein response;endoplasmic-reticulum;epithelial-cells;cyclosporine-a;ca2+ stores;nf-at;death;stress||Project:||Apoptosis||期刊/報告no：:||Apoptosis, Volume 11, Issue 12, Page(s) 2167-2177.||摘要:||
Aristolochic acid (AA) has been demonstrated to play a causal role in Chinese herbs nephropathy. However, the detailed mechanism for AA to induce apoptosis of renal tubular cells remains obscure. In this study, we show that AA evokes a rapid rise in the intracellular Ca2+ concentration of renal tubular cells through release of intracellular endoplasmic reticulum Ca2+ stores and influx of extracellular Ca2+, which in turn causes endoplasmic reticulum stress and mitochondria stress, resulting in activation of caspases and finally apoptosis. Ca2+ antagonists, including calbindin-D-28k (an intracellular Ca2+ buffering protein) and BAPTA-AM (a cell-permeable Ca2+ chelator), are capable of ameliorating endoplasmic reticulum stress and mitochondria stress, and thereby enhance the resistance of the cells to AA. Moreover, we show that overexpression of the anti-apoptotic protein Bcl-2 in combination with BAPTA-AM treatment can provide renal tubular cells with almost full protection against AA-induced cytotoxicity. In conclusion, our results demonstrate an impact of AA to intracellular Ca2+ concentration and its link with AA-induced cytotoxicity.
|Appears in Collections:||生命科學院|
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