BAG-1L Protects SH-SY5Y Neuroblastoma Cells Against Hypoxia/Re-oxygenation Through Up-Regulating HSP70 and Activating PI3K/AKT Signaling Pathway

被引:24
作者
Wang, Yun [1 ]
Jia, Chao [2 ]
Li, Qing-Shu [2 ]
Xie, Chun-Yu [1 ]
Zhang, Nan [1 ]
Qu, Yan [2 ]
机构
[1] Qingdao Univ, Med Coll, Sch Nursing, Qingdao 266021, Shandong, Peoples R China
[2] Qingdao Univ, Affiliated Qingdao Municipal Hosp, Dept Intens Care Unit, Qingdao 266071, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
BAG-1L gene; HSP70; Hypoxia; Antiapoptotic effect; PI3K/AKT pathway; NEURONAL SURVIVAL; EXPRESSION; KINASE; BAG1; DEATH; BRAIN; BCL-2;
D O I
10.1007/s11064-017-2304-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BCL-2-associated athanogene-1(BAG-1) is a multifunctional and anti-apoptotic protein that was first identified as a binding partner of BCL-2. But the effects and mechanisms for BAG-1 against hypoxic damage is unclear up to now. Whether BAG-1 could protect the human brain against hypoxic damage through up-regulating 70 kDa heat shock proteins (HSP70) and PI3K/AKT pathway activation? In present study, we examined the changes of HSP70 and AKT and p-AKT protein level in SH-SY5Y cells with BAG-1L gene over-expression subjected to hypoxia/reoxygenation injury. BAG-1L over-expression increased neuronal viability, and it reduced apoptosis of neurons after hypoxia/re-oxygenation for 8 h. BAG-1L over-expression enhanced the HSP70 protein levels and increased p-AKT/total AKT ratio after hypoxia/re-oxygenation for 8 h. These results suggest that BAG-1L over-expression protects against hypoxia/re-oxygenation injury, at least in part, by interacting with HSP70, and by accelerating the activation of PI3K/AKT pathways.
引用
收藏
页码:2861 / 2868
页数:8
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