Hsp20 Protects against Oxygen-Glucose Deprivation/Reperfusion-Induced Golgi Fragmentation and Apoptosis through Fas/FasL Pathway.
Hsp20 Protects against Oxygen-Glucose Deprivation/Reperfusion-Induced Golgi Fragmentation and Apoptosis through Fas/FasL Pathway.
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Hsp20 通过 Fas/FasL 途径防止缺氧/葡萄糖剥夺/再灌注诱导的高尔基体断裂和细胞凋亡。
DOI：
10.1155/2015/606934
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发表时间：
2015
影响因子：
--
通讯作者：
Zeng L
中科院分区：
文献类型：
--
作者：
Zhong B;Hu Z;Tan J;Lu T;Lei Q;Chen C;Zeng L
脑缺血再灌注损伤在急性缺血性脑卒中后组织损伤的发生发展中起重要作用。寻找有效的神经保护剂已成为治疗缺血性脑卒中的首要任务。高尔基体（GA）是脑缺血再灌注损伤的重要细胞器，其保护作用是脑缺血再灌注损伤治疗的重要靶点。在缺血再灌注损伤模型中评估了Hsp 20对GA的保护作用，Hsp 20是一种潜在的细胞保护剂，由于其分子伴侣样活性和参与调节许多重要过程。小鼠神经母细胞瘤Neuro 2a（N2 a）细胞经受氧-葡萄糖剥夺/再灌注（OGDR）损伤。OGDR诱导N2 a细胞中高尔基体断裂、凋亡和p115裂解。然而，转染Hsp 20显着减弱OGDR诱导的高尔基体断裂和凋亡。Hsp 20与Bax相互作用，降低FasL和Bax表达，并抑制暴露于OGDR的N2 a细胞中的caspase 3和p115切割。我们的数据表明，增加Hsp 20的表达保护对OGDR诱导的高尔基体断裂和凋亡，可能通过与Bax的相互作用和随后的改善OGDR诱导的p115裂解通过Fas/FasL信号通路的升高。Hsp 20对OGDR损伤的神经保护潜力及其潜在机制将为其在脑缺血再灌注相关疾病中的潜在临床应用铺平道路。
Cerebral ischemia-reperfusion injury plays an important role in the development of tissue injury after acute ischemic stroke. Finding effective neuroprotective agents has become a priority in the treatment of ischemic stroke. The Golgi apparatus (GA) is a pivotal organelle and its protection is an attractive target in the treatment of cerebral ischemia-reperfusion injury. Protective effects of Hsp20, a potential cytoprotective agent due to its chaperone-like activity and involvement in regulation of many vital processes, on GA were assessed in an ischemia-reperfusion injury model. Mouse neuroblastoma Neuro2a (N2a) cells were subjected to oxygen-glucose deprivation/reperfusion (OGDR) insult. OGDR induces Golgi fragmentation, apoptosis, and p115 cleavage in N2a cells. However, transfection with Hsp20 significantly attenuates OGDR-induced Golgi fragmentation and apoptosis. Hsp20 interacts with Bax, decreases FasL and Bax expression, and inhibits caspases 3 and p115 cleavage in N2a cells exposed to OGDR. Our data demonstrate that increased Hsp20 expression protects against OGDR-induced Golgi fragmentation and apoptosis, likely through interaction with Bax and subsequent amelioration of the OGDR-induced elevation in p115 cleavage via the Fas/FasL signaling pathway. This neuroprotective potential of Hsp20 against OGDR insult and the underlying mechanism will pave the way for its potential clinical application for cerebral ischemia-reperfusion related disorders.
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影响因子：
5
作者：
Fan GC;Kranias EG
通讯作者：
Kranias EG
影响因子：
5.2
作者：
Wang, Xiaohong;Zhao, Tiemin;Huang, Wei;Wang, Tao;Qian, Jiang;Xu, Meifeng;Kranias, Evangelia G.;Wang, Yigang;Fan, Guo-Chang
通讯作者：
Fan, Guo-Chang
DOI：
10.1073/pnas.1220978110
发表时间：
2013-01-22
影响因子：
11.1
作者：
Thayer, Desiree A.;Jan, Yuh Nung;Jan, Lily Yeh
通讯作者：
Jan, Lily Yeh
影响因子：
12.7
作者：
Sakurai, A;Okamoto, K;Gonatas, NK
通讯作者：
Gonatas, NK
DOI：
10.1083/jcb.200208013
发表时间：
2002-11-25
期刊：
The Journal of cell biology
影响因子：
--
作者：
Chiu R;Novikov L;Mukherjee S;Shields D
通讯作者：
Shields D