Nucleocapsid Protein of SARS-CoV-2 Upregulates RANTES Expression in A172 Glioblastoma Cells
Bakhytgul Gadilgereyeva, Zhanar Kunushpayeva, Mira Abdrakhmanova, Aizere Khassenova, Nail Minigulov, Timo Burster, Olena Filchakova
TL;DR
This study shows that the nucleocapsid protein of SARS-CoV-2 increases RANTES chemokine levels in glioblastoma cells without affecting cell viability or migration.
Contribution
The novel finding is that the SARS-CoV-2 nucleocapsid protein upregulates RANTES in glial-derived A172 cells.
Findings
Exposure to SARS-CoV-2 nucleocapsid protein upregulates RANTES at both mRNA and protein levels in A172 cells.
The nucleocapsid protein does not affect cell viability or migration in these cells.
Abstract
SARS-CoV-2, the pathogenic virus that induces COVID-19 disease, contains four structural proteins in its virion. The nucleocapsid (N) protein is one of the four structural proteins that play a crucial role in the assembly of viral RNA into ribonucleoprotein. In addition, the N protein contributes to viral pathogenesis. One of the functions attributed to the N protein is the triggering of cytokine release by lung epithelial cells, macrophages, and monocytes. This study addresses the cellular effects of the N protein of SARS-CoV-2 on cells of glial origin. We report the upregulation of the RANTES chemokine in A172 glioblastoma cells at both the mRNA and protein levels in response to exposure to SARS-CoV-2 nucleocapsid protein. The N protein did not have an effect on cell viability and cell migration.
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Taxonomy
TopicsSARS-CoV-2 and COVID-19 Research · Long-Term Effects of COVID-19 · COVID-19 Clinical Research Studies