Arutyunov, A.; Durán-Laforet, V.; Ai, S.; Ferrari, L.; Murphy, R.; Schafer, D.P.; Klein, R.S. West Nile Virus-Induced Expression of Senescent Gene Lgals3bp Regulates Microglial Phenotype within Cerebral Cortex. Biomolecules2024, 14, 808.
Arutyunov, A.; Durán-Laforet, V.; Ai, S.; Ferrari, L.; Murphy, R.; Schafer, D.P.; Klein, R.S. West Nile Virus-Induced Expression of Senescent Gene Lgals3bp Regulates Microglial Phenotype within Cerebral Cortex. Biomolecules 2024, 14, 808.
Arutyunov, A.; Durán-Laforet, V.; Ai, S.; Ferrari, L.; Murphy, R.; Schafer, D.P.; Klein, R.S. West Nile Virus-Induced Expression of Senescent Gene Lgals3bp Regulates Microglial Phenotype within Cerebral Cortex. Biomolecules2024, 14, 808.
Arutyunov, A.; Durán-Laforet, V.; Ai, S.; Ferrari, L.; Murphy, R.; Schafer, D.P.; Klein, R.S. West Nile Virus-Induced Expression of Senescent Gene Lgals3bp Regulates Microglial Phenotype within Cerebral Cortex. Biomolecules 2024, 14, 808.
Abstract
Microglia, the resident macrophages of the central nervous system, exhibit altered gene expression in response to various neurological conditions. This study investigates the relationship between West Nile Virus infection, and microglial senescence, focusing on the role of LGALS3BP, a protein implicated in both antiviral responses and aging. Us-ing spatial transcriptomics, RNA sequencing and flow cytometry, we characterized changes in microglial gene signatures in adult and aged mice following recovery from WNV encephalitis. Additionally, we analyzed Lgals3bp expression and generated Lgals3bp-deficient mice to assess the impact on neuroinflammation and microglial phe-notypes. Our results show that WNV-activated microglia share transcriptional signa-tures with aged microglia, including upregulation of genes involved in interferon re-sponse and inflammation. Lgals3bp was broadly expressed in the CNS and robustly up-regulated during WNV infection and aging. Lgals3bp-deficient mice exhibited reduced neuroinflammation, increased homeostatic microglial numbers, and altered T cell popu-lations without differences in virologic control or survival. This data indicates that LGALS3BP has a role in regulating neuroinflammation and microglial activation and suggest that targeting LGALS3BP might provide a potential route for mitigating neu-roinflammation-related cognitive decline in aging and post-viral infections.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
,
