Bone marrow stromal cell-derived growth inhibitor serves as a stress sensor to induce autophagy
Bone marrow stromal cell-derived growth inhibitor serves as a stress sensor to induce autophagy
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骨髓基质细胞源性生长抑制剂作为应激传感器诱导自噬
DOI：
10.1002/1873-3468.13732
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发表时间：
2020
期刊：
影响因子：
3.5
通讯作者：
Xia Dajing
中科院分区：
文献类型：
--
作者：
Zhang Jianbin;Wang Liming;Xu Jian;Tang Yancheng;Huang Bo;Chen Zhifeng;Zhang Ting;Shen Han-Ming;Wu Yihua;Xia Dajing
自噬是一种进化上保守的应激反应，其促进细胞内组分的溶酶体降解。骨髓基质细胞衍生的生长抑制剂（BDGI）作为一种应激传感器，可通过氧化应激和DNA损伤上调。然而，BDGI在某些应激自噬反应中的作用仍然未知。在这里，我们的研究结果表明，BDGI定义了压力下自噬诱导的影响。BDGI的过表达促进自噬，而BDGI的敲低损害自噬。从机制上讲，BDGI定位于细胞核并与转录因子EB相互作用，以增加多种自噬和溶酶体相关基因的表达。此外，BDGI以p53依赖性方式调节自噬。此外，BDGI诱导的自噬使细胞能够在应激条件下存活。总之，我们的研究表明BDGI是一种积极调节自噬的压力传感器。
Autophagy is an evolutionarily conserved stress response that promotes the lysosomal degradation of intracellular components. The bone marrow stromal cell‐derived growth inhibitor (BDGI) functions as a stress sensor which is upregulated by oxidative stress and DNA damage. However, the role of BDGI in autophagic response to certain stresses remains unknown. Here, our results demonstrate that BDGI defines the impact of autophagy induction under stresses. Overexpression of BDGI promotes, while knockdown of BDGI impairs, autophagy. Mechanistically, BDGI localizes to the nucleus and interacts with the transcription factor transcription factor EB to increase the expression of multiple autophagy‐ and lysosome‐related genes. In addition, BDGI regulates autophagy in a p53‐dependent manner. Furthermore, BDGI‐induced autophagy enables cell survival under stress conditions. Taken together, our study demonstrates that BDGI is a stress sensor that positively regulates autophagy.