Next Article in Journal
Directed Evolution of an Improved Rubisco; In Vitro Analyses to Decipher Fact from Fiction
Previous Article in Journal
Comparing the Osteogenic Potentials and Bone Regeneration Capacities of Bone Marrow and Dental Pulp Mesenchymal Stem Cells in a Rabbit Calvarial Bone Defect Model
Open AccessArticle

Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection

1
Center for Research and Innovation, Faculty of Medical Technology, Mahidol University, Salaya, Nakhon Pathom 73170, Thailand
2
Chulabhorn Graduate Institute, Chulabhorn Royal Academy, Bangkok 10210, Thailand
3
Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhon Pathom 73170, Thailand
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(20), 5016; https://doi.org/10.3390/ijms20205016
Received: 9 September 2019 / Revised: 6 October 2019 / Accepted: 8 October 2019 / Published: 10 October 2019
(This article belongs to the Special Issue Molecular Research on Arboviruses Infection)
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. View Full-Text
Keywords: Japanese encephalitis virus; kinetic viral replication; neuronal cell death; apoptosis; Bcl-2; Bax Japanese encephalitis virus; kinetic viral replication; neuronal cell death; apoptosis; Bcl-2; Bax
Show Figures

Figure 1

MDPI and ACS Style

Wongchitrat, P.; Samutpong, A.; Lerdsamran, H.; Prasertsopon, J.; Yasawong, M.; Govitrapong, P.; Puthavathana, P.; Kitidee, K. Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection. Int. J. Mol. Sci. 2019, 20, 5016.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop