Expression changes of the notch signaling pathway of PC12 cells after oxygen glucose deprivation

被引:7
|
作者
Xu, Zhong-Xin [1 ]
Xu, Lei [1 ]
Wang, Jiao-Qi [1 ]
Mang, Jing [1 ]
Yang, Le [2 ]
He, Jin-Ting [1 ]
机构
[1] Jilin Univ, China Japan Union Hosp, Dept Neurol, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China
[2] Peoples Hosp Jilin Prov, Changchun 130021, Jilin, Peoples R China
关键词
Notch signaling; Oxygen glucose deprivation model (OGD); PC12; cells; Nerve growth factor (NGF); NEURAL PROGENITORS; APOPTOSIS; GROWTH; MODEL; NEUROGENESIS; STROKE; CANCER;
D O I
10.1016/j.ijbiomac.2018.07.039
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
Ischemic stroke is caused by obstructed blood supply to the brain. It is a common as well as a serious health problem worldwide, which is often linked to disability and mortality. Here we studied, under the conditions of oxygen glucose deprivation (OGD), the expression of Notch signaling pathway proteins in PC12 cells. K12 cells were stimulated and converted into neuron-like cells by nerve growth factor. Exposure to OGD was used as an in vitro model of cerebral hypoxia-ischemia. Our findings demonstrate that, after 3 h of OGD exposure, the expression of Notch1, Hes1 and Hes5 significantly increased, on both mRNA and protein levels. This effect gradually reduced with continuous OGD treatment, but the expression levels of these three genes remained higher, compared to untreated controls, even after 24 h of OGD exposure. Our results suggest that OGD exposure up-regulates the expression of Notchl, Hes1 and Hes5, which are important participants in Notch signaling pathway. Since their regulatory roles appear to change dynamically with the extension of OGD, the activation of the Notch pathway may play an important role in cerebral ischemic injury. (C) 2018 Elsevier BV. All rights reserved.
引用
收藏
页码:1984 / 1988
页数:5
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