ArticleOpen veterinary journal2025
Apoptotic role of RASSF6 in regulating PRV-infected porcine alveolar macrophages.
Article in Open veterinary journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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Abstract
Background: Pseudorabies virus (PRV), a zoonotic swine alphaherpesvirus, poses a severe threat to global pig production and public health. Aim: This study aimed to investigate the regulatory role of the RASSF6 gene in PRV-infected porcine alveolar macrophages (3D4/21). Methods: We established stable cellular models of RASSF6 overexpression (verified by qRT-PCR and immunofluorescence using an empty vector control) and siRNA-mediated RASSF6 silencing (verified by qRT-PCR) to investigate the role of RASSF6. Using these models, we assessed viral replication (quantified by qRT-PCR/TCID Results: RASSF6 expression was significantly upregulated after PRV infection. RASSF6 overexpression inhibited 3D4/21 cell proliferation and PRV replication and promoted apoptosis through Bax and Caspase-3/9 activation. RASSF6 silencing promoted cell proliferation and viral replication and inhibited apoptosis. Conclusion: RASSF6 is a critical host defense factor against PRV infection in porcine alveolar macrophages. RASSF6 upregulation restricts viral replication by inducing apoptosis via Bax/caspase-3/9 activation and simultaneously suppressing cell proliferation. Conversely, RASSF6 silencing creates a permissive environment for PRV propagation by inhibiting apoptosis and enhancing cell survival. These findings reveal RASSF6-mediated apoptosis as a novel antiviral mechanism and highlight its potential as a therapeutic target for controlling PRV pathogenesis.
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