A proteomic network approach across the kidney stone disease reveals endoplasmic reticulum stress and crystal-cell interaction in kidney.
A proteomic network approach across the kidney stone disease reveals endoplasmic reticulum stress and crystal-cell interaction in kidney.
复制标题
肾结石疾病的蛋白质组网络方法揭示了肾脏中的内质网应激和晶体细胞相互作用。
DOI:
10.1155/2019/9307256
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发表时间:
2019
影响因子:
--
通讯作者:
Bing Gao
中科院分区:
文献类型:
--
作者:
Baoyu Yang;Xiuli Lu;Yang Li;Yuanyuan Li;Daojun Yu;Weiwen Zhang;Chaojie Duan;Kazumi Taguchi;Takahiro Yasui;Kenjiro kohri;Bing Gao
Crystal‐cell interactions are a vital step toward kidney stone formation. However, its mechanisms remained unclear. Here, a protein‐protein interaction (PPI) network analysis of a kidney stone revealed that the proteins were enriched in a posttranslational protein modification process in the endoplasmic reticulum (ER). Thein vitrostudy showed that the markers of ER stress, including Bip and CHOP, were upregulated, PERK and ATF6 were activated, and XBP‐1 mRNA was spliced. An ER stress‐specific protein, caspase‐12, was activated in the apoptotic cells induced by calcium oxalate monohydrate (COM) crystals. The treatment with tunicamycin, an ER stress inducer, promoted the crystal‐cell adhesion assayed by atomic absorption, reduced cell viability assayed by MTT, and downregulated the expression of proteins involved in the crystal formations. The treatment with salubrinal, an ER stress inhibitor, reversed the above effects for both tunicamycin and COM crystals. The aforementioned main observations were supported byin vivostudy. These data demonstrated that ER stress was an essentially biological process of crystal‐cell interactions. Our findings suggest that blocking ER stress may become a potential approach to preventing a kidney stone.