Publication: Screening of pro-apoptotic genes upregulated in an experimental street rabies virus-infected neonatal mouse brain
Issued Date
2005-01-01
Resource Type
ISSN
03855600
Other identifier(s)
2-s2.0-20444372303
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Microbiology and Immunology. Vol.49, No.5 (2005), 423-431
Suggested Citation
Sukathida Ubol, Jitra Kasisith, Dhanesh Pitidhammabhorn, Veera Tepsumethanol Screening of pro-apoptotic genes upregulated in an experimental street rabies virus-infected neonatal mouse brain. Microbiology and Immunology. Vol.49, No.5 (2005), 423-431. doi:10.1111/j.1348-0421.2005.tb03746.x Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/16618
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Screening of pro-apoptotic genes upregulated in an experimental street rabies virus-infected neonatal mouse brain
Other Contributor(s)
Abstract
Rabies virus (RABV) is able to induce apoptotic death of target cells. The molecular pathway of RABV-induced cell death is partially known. In the present study, cDNA array analysis was used as a tool to screen for pro-apoptotic genes that may be involved in RABV induction. RNA was extracted from the infected CNS and from mock-infected controls. When the mean gene expression was compared between the infected group and controls, 21 potential apoptotic genes were identified that exhibited more than 2.5-fold difference in their expression levels. These 21 genes can be grouped into two groups, those genes that participate in the commitment phase and those that play a role as executioners. Examples of genes in commitment phase were death receptors (Fas-L receptor, TNF-receptor), lysosomal proteases, calpain, caspase-1, signaling molecules (ERK, p38MAPK) and bcl-2 family members. Cytochrome c and caspase-3 were representatives of executioners. Based on types of genes activated during the commitment phase, two independent apoptotic mechanisms may be activated in response to the RV infection. The first is immune-mediated death which may operate through the receptor-ligand pathway activated by caspase-1 and the pro-inflammatory cytokine, IL-1β. The other mechanism is a protease-mediated process which involves lysosomal proteases and calcium-dependent neutral proteases. These two stimulating pathways were followed by Bad, Bak, Bid activation and subsequently the upregulation of cytochrome c and caspase-3. In addition, mobilization of K+ion and other accessory apoptotic genes such as annexins and clusterin were also upregulated.