Publication: Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection
Issued Date
2019-10-10
Resource Type
ISSN
14220067
Other identifier(s)
2-s2.0-85074238959
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
International journal of molecular sciences. Vol.20, No.20 (2019)
Suggested Citation
Prapimpun Wongchitrat, Arisara Samutpong, Hatairat Lerdsamran, Jarunee Prasertsopon, Montri Yasawong, Piyarat Govitrapong, Pilaipan Puthavathana, Kuntida Kitidee Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection. International journal of molecular sciences. Vol.20, No.20 (2019). doi:10.3390/ijms20205016 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/50055
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection
Other Contributor(s)
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.