Academic Journal

p21-Activated Kinase 4 Signaling Promotes Japanese Encephalitis Virus-Mediated Inflammation in Astrocytes

التفاصيل البيبلوغرافية
العنوان: p21-Activated Kinase 4 Signaling Promotes Japanese Encephalitis Virus-Mediated Inflammation in Astrocytes
المؤلفون: Wen He, Zikai Zhao, Awais Anees, Yunchuan Li, Usama Ashraf, Zheng Chen, Yunfeng Song, Huanchun Chen, Shengbo Cao, Jing Ye
المصدر: Frontiers in Cellular and Infection Microbiology, Vol 7 (2017)
بيانات النشر: Frontiers Media S.A., 2017.
سنة النشر: 2017
المجموعة: LCC:Microbiology
مصطلحات موضوعية: JEV, PAK4, inflammation, MAPK, astrocyte, Microbiology, QR1-502
الوصف: Japanese encephalitis virus (JEV) targets central nervous system, resulting in neuroinflammation with typical features of neuronal death along with hyper activation of glial cells. Exploring the mechanisms responsible for the JEV-caused inflammatory response remains a pivotal area of research. In the present study, we have explored the function of p21-activated kinase 4 (PAK4) in JEV-mediated inflammatory response in human astrocytes. The results showed that JEV infection enhances the phosphorylation of PAK4 in U251 cells and mouse brain. Knockdown of PAK4 resulted in decreased expression of inflammatory cytokines that include tumor necrosis factor alpha, interleukin-6, interleukin-1β, and chemokine (C-C motif) ligand 5 and interferon β upon JEV infection, suggesting that PAK4 signaling promotes JEV-mediated inflammation. In addition, we found that knockdown of PAK4 led to the inhibition of MAPK signaling including ERK, p38 MAPK and JNK, and also resulted in the reduced nuclear translocation of NF-κB and phosphorylation of AP-1. These results demonstrate that PAK4 signaling actively promotes JEV-mediated inflammation in human astrocytes via MAPK-NF-κB/AP-1 pathway, which will provide a new insight into the molecular mechanism of the JEV-induced inflammatory response.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2235-2988
Relation: http://journal.frontiersin.org/article/10.3389/fcimb.2017.00271/full; https://doaj.org/toc/2235-2988
DOI: 10.3389/fcimb.2017.00271
URL الوصول: https://doaj.org/article/dc6aa16978e740bebe93964a0fa7166a
رقم الانضمام: edsdoj.6aa16978e740bebe93964a0fa7166a
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:22352988
DOI:10.3389/fcimb.2017.00271