Research Papers:

The impact of neuronal Notch-1/JNK pathway on intracerebral hemorrhage-induced neuronal injury of rat model

Maohua Chen, Jun Sun _, Chuan Lu, Xiandong Chen, Huajun Ba, Qun Lin, Jianyong Cai and Junxia Dai

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Oncotarget. 2016; 7:73903-73911. https://doi.org/10.18632/oncotarget.12094

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Maohua Chen1, Jun Sun1, Chuan Lu1, Xiandong Chen1, Huajun Ba1, Qun Lin1, Jianyong Cai1, Junxia Dai1

1Department of Neurosurgery, Wenzhou Central Hospital, Affiliated Dingli Clinical Institute of Wenzhou Medical University, Wenzhou, China

Correspondence to:

Jun Sun, email: [email protected]

Keywords: Notch-1, JNK/c-Jun, ICH, Rat

Received: June 29, 2016     Accepted: September 05, 2016     Published: September 17, 2016


Notch signaling is a highly conserved pathway that regulates cell fate decisions during embryonic development. Notch activation endangers neurons by modulating NF-κB and HIF-1α pathways, however, the role of Notch signaling in activating JNK/c-Jun following intracerebral hemorrhage (ICH) has not been investigated. In this study, we used rat ICH models and thrombin-induced cell models to investigate the potential role of Notch-1/JNK signals. Our findings revealed that Notch-1 and JNK increased in hematoma-surrounding neurons tissues following ICH during ischemic conditions (all p<0.05). Besides, the expression of active caspase-3 protein was also up-regulated after ICH. According to in-vitro assays, the expression of Notch-1, p-JNK, and active caspase-3 were all up-regulated in cell viability-decreasing ICH cell models (all p<0.05). However, blocking of either Notch-1 or JNK suppressed the phosphorylation of JNK and the expression of active caspase-3, and cell viability was obviously ameliorated. In conclusion, this work suggested Notch-1 activates JNK pathway to induce the active caspase-3, leading to neuronal injury when intracerebral hemorrhage or ischemia occurred. Thus the Notch-1/JNK signal pathway has an important role in ICH process, and may be a therapeutic target to prevent brain injury.

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