Hypoxia-induced autophagy promotes human prostate stromal cells survival and ER-stress
Hypoxia-induced autophagy promotes human prostate stromal cells survival and ER-stress
复制标题
缺氧诱导的自噬促进人前列腺基质细胞存活和内质网应激
DOI：
10.1016/j.bbrc.2015.07.086
复制
发表时间：
2015-09-04
影响因子：
3.1
通讯作者：
Chen, Ji-Min
中科院分区：
文献类型：
--
作者：
Zhang, Nan;Ji, Na;Chen, Ji-Min
良性前列腺增生症（BPH）是严重威胁老年男性健康的常见疾病之一。越来越多的证据表明低氧可诱发BPH。然而，低氧诱导BPH的潜在机制尚不清楚。在本研究中，低氧诱导的自噬可促进WPMY-1细胞的存活和内质网应激（ER应激）。自噬抑制剂（3-甲基腺嘌呤、巴弗洛霉素A1）或siRNA干扰自噬基因（Beclin 1、ATG 5）均能降低缺氧诱导的WPMY-1细胞存活率。此外，缺氧处理后的WPMY-1细胞存在内质网应激，而C/EBP同源蛋白siRNA（CHOP）是内质网应激途径中的重要蛋白，可抑制自噬和细胞存活。总之，我们的数据支持了一种新的模型，即自噬作为细胞保护反应，通过ER应激促进人前列腺基质细胞在缺氧条件下的细胞存活。(C)2015 Elsevier Inc. All rights reserved.
Benign prostatic hyperplasia (BPH) is emerging as one of the most common diseases seriously threatening the health of elderly men. Accumulating evidences indicate that hypoxia could induce BPH. However, the underlying mechanism of BPH induced by hypoxia is not clear. In the study, hypoxia-induced autophagy could promote cell survival and endoplasmic reticula stress (ER stress) in WPMY-1 cells. Cell viability induced by hypoxia could been decreased by autophagy inhibitors (3-methyladenine, bafilomycin A1) or siRNA interference in two autophagy genes (Beclin1, ATG5) in WPMY-1 cells. Furthermore, ER stress was present in hypoxia-treated WPMY-1 cells, while autophagy and cell survival could been inhibited by C/EBP-homologous protein siRNA (CHOP), which is an important protein of ER stress pathway. Taken together, our data support a novel model that autophagy as a cytoprotective response promotes cell survival via ER stress under hypoxia in human prostate stromal cells. (C) 2015 Elsevier Inc. All rights reserved.