Simple jQuery Dropdowns
Please use this identifier to cite or link to this item:
Title: Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection
Authors: Prapimpun Wongchitrat
Arisara Samutpong
Hatairat Lerdsamran
Jarunee Prasertsopon
Montri Yasawong
Piyarat Govitrapong
Pilaipan Puthavathana
Kuntida Kitidee
Mahidol University
Chulabhorn Royal Academy
Keywords: Biochemistry, Genetics and Molecular Biology;Chemical Engineering;Chemistry;Computer Science
Issue Date: 10-Oct-2019
Citation: International journal of molecular sciences. Vol.20, No.20 (2019)
Abstract: Japanese encephalitis virus (JEV) infection induces uncontrolled neuronal apoptosis, leading to irreversible brain damage. However, the mechanism of JEV-induced neuronal apoptosis has not been clearly elucidated. This study aimed to investigate both virus replication and neuronal cell apoptosis during JEV infection in human neuroblastoma SH-SY5Y cells. As a result, the kinetic productions of new viral progeny were time- and dose-dependent. The stimulation of SH-SY5Y cell apoptosis was dependent on the multiplicity of infections (MOIs) and infection periods, particularly during the late period of infection. Interestingly, we observed that of full-length Bax (p21 Bax) level started to decrease, which corresponded to the increased level of its cleaved form (p18 Bax). The formation of p18 Bax resulting in cytochrome c release into the cytosol appeared to correlate with JEV-induced apoptotic cell death together with the activation of caspase-3/7 activity, especially during the late stage of a robust viral infection. Therefore, our results suggest another possible mechanism of JEV-induced apoptotic cell death via the induction of the proteolysis of endogenous p21 Bax to generate p18 Bax. This finding could be a new avenue to facilitate novel drug discovery for the further development of therapeutic treatments that could relieve neuronal damage from JEV infection.
ISSN: 14220067
Appears in Collections:Scopus 2019

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.