Niban protein regulates apoptosis in HK-2 cells via caspase-dependent pathway
Niban protein regulates apoptosis in HK-2 cells via caspase-dependent pathway
复制标题
Niban蛋白通过caspase依赖性途径调节HK-2细胞凋亡
DOI：
10.1080/0886022x.2019.1619582
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发表时间：
2019-01-01
期刊：
影响因子：
3
通讯作者：
Zhang, Hao
中科院分区：
文献类型：
--
作者：
Tang, Shiqi;Wang, Jianwen;Zhang, Hao
摘要目的：探讨Niban蛋白是否通过调控肾小管上皮细胞凋亡在肾间质纤维化中发挥作用并探讨其机制。研究方法：采用C57 B/6 J小鼠建立单侧输尿管梗阻（UUO）模型，分为假手术组、3、7、14 d组。免疫组化和Western blot检测Niban的表达。TUNEL法检测细胞凋亡。将Niban siRNA和过表达Niban质粒分别转染HK-2细胞，探讨Niban在血管紧张素II（AngII）和内质网（ER）应激损伤中的凋亡相关机制。结果：随着梗阻程度的加重，尼班的表达逐渐减少，细胞凋亡逐渐增多。沉默Niban不仅增加了AngII和ER应激诱导的细胞凋亡，而且还促进了caspase 8、caspase 9、Bip和Chop的表达。Niban的过表达减少AngII诱导的细胞凋亡和caspase 8和caspase 9的表达。结论：Niban蛋白参与了HK-2细胞的凋亡调控，并可能通过caspase依赖的途径。
Abstract Purpose: To investigate whether Niban protein plays a role in renal interstitial fibrosis by regulating renal tubular epithelial cell apoptosis and explore the underlying mechanism. Methods: Unilateral ureteral obstruction (UUO) model was performed in C57B/6J mice, and divided into sham operation group and groups of days 3, days 7, and days 14. Niban expression was detected by immunohistochemistry and Western blot. TUNEL assays were used to detected apoptosis. Niban siRNA and overexpression Niban plasmid were transfected in HK-2 cells respectively to explore apoptosis related mechanisms of Niban during angiotensin II (AngII) – and endoplasmic reticulum (ER) stress-induced injury. Results: With the development of obstruction, Niban’s expression decreased gradually while apoptosis increased. Silencing of Niban not only increased the AngII- and ER stress-induced apoptosis, but also promoted the expression of caspase 8, caspase 9, Bip, and Chop. Overexpression of Niban reduced AngII-induced apoptosis and the expression of caspase 8 and caspase 9. Conclusions: Niban protein is involved in apoptosis regulation in HK-2 cells, and most likely via caspase-dependent pathway.