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Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells 期刊论文

编号：

b4daf0c4-d1de-449d-b52b-91155cb9f155
作者：

Ge, Zehe^[1,2];Diao, Haipeng^[1,2];Ji, Xiaoli^[1,2];Liu, Qingping^[1,2];Zhang, Xiaoyan(章晓燕)*^[3,4,5]Wu, Qing(吴庆)*^[1,2]
语种：

English
期刊：

TOXICOLOGY LETTERS ISSN：0378-4274 2018 年 288 卷 (35 - 43) ; MAY 15
收录：
关键词：

Cadmium HK-2 cells GJIC ER stress AKT signaling
摘要：

Cadmium (Cd), a toxic heavy metal, is known to induce renal toxicity by primarily targeting at renal proximal tubule. Endoplasmic reticulum (ER) stress and gap junctional intercellular communication (GJIC) regulate many pathophysiological processes. Yet, how ER stress and GJIC regulate Cd-induced nephrotoxicity remain elusive. In this study, we treated human proximal tubule (HK-2) cells with 1 mu M CdCl2 every other day for 12 days and found that Cd significantly increased cell apoptosis at 10 and 12 days. This cytotoxicity correlated with activation of ER stress and apoptotic signaling evidenced by upregulation of inositol-requiring enzyme 1 (IRE1 alpha), splice X-box binding protein-1 (XBP-1s), and apoptosis signal-regulating kinase 1 (ASK1) proteins. Interestingly, the AKT signaling was activated at 2- and 4-day and then inhibited at 10- and 12-day of Cd treatment; by contrast, Cd decreased GJIC levels at 2- and 4-day followed by a significant increase at 10- and 12-day treatment. Activation of AKT by SC79 or inhibition of GJIC by 18 alpha-glycyrrhetinic acid (18 alpha-GA) completely abolished Cd-induced AKT inhibition and IRE1 alpha-ASK1 activation. Importantly, pretreatment with ER stress inhibitor or 18 alpha-GA significantly mitigated Cd-induced apoptosis. These results suggest that GJIC collaborates with AKT signaling and ER stress in regulating prolonged Cd-treatment-induced apoptosis in HK-2 cells.
推荐引用方式
GB/T 7714：

Ge Zehe,Diao Haipeng,Ji Xiaoli, et al. Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells [J].TOXICOLOGY LETTERS,2018,288:35-43.
APA：

Ge Zehe,Diao Haipeng,Ji Xiaoli,Liu Qingping,&Wu Qing.(2018).Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells .TOXICOLOGY LETTERS,288:35-43.
MLA：

Ge Zehe, et al. "Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells" .TOXICOLOGY LETTERS 288(2018):35-43.

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