AI Article Synopsis
- This study investigated how Goose parvovirus (GPV) and its NS1 protein lead to apoptosis (cell death) in goose embryo fibroblast (GEF) cells.
- Results showed that GPV infection significantly increased apoptosis rates and viral load, with specific changes in mitochondrial function and AIF expression.
- The research identified that the AIF-mediated pathway contributes to apoptosis, highlighting the roles of mitochondrial membrane potential, reactive oxygen species (ROS), and cathepsin D activities in this process.
Article Abstract
In this study, the effects of Goose parvovirus (GPV) infection as well as the possible role of NS1 protein on apoptosis induction in goose embryo fibroblast (GEF) cells were examined. Flow cytometry analysis and TUNEL assays revealed that GPV infection and NS1 transfection induced significant apoptosis in GEF cells compared to what was observed in mock-infected cells. Interestingly, the increase in the rate of apoptosis detected in GPV-infected GEFs was accompanied by an increased viral load in the cells. In addition, the apoptotic pathway was mediated by apoptosis-inducing factors (AIFs) and internal factors that influence the release of AIFs. The results indicated that the mitochondrial membrane potential was decreased, and AIF expression was increased in the nucleus (P < 0.01). Reactive oxygen species (ROS) increased gradually within 48 h (P < 0.001). Cathepsin D activities were also increased (P < 0.05). The results demonstrated that the AIF-mediated pathway is a new mitochondrial apoptotic pathway and that mitochondrial depolarization, ROS content, and cathepsin D activities are the key factors influencing apoptosis in GEF cells.
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| http://dx.doi.org/10.1016/j.rvsc.2021.04.018 | DOI Listing |
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