Severe and post-COVID-19 are associated with high expression of vimentin and reduced expression of N-cadherin.

SARS-CoV-2 penetrates human cells via its spike protein, which mainly interacts with ACE2 receptors, triggering viral replication and an exacerbated immune response characterized by a cytokine storm. Vimentin III, an intermediate filament protein predominantly found in mesenchymal cells, has garnered considerable attention in recent research due to its multifaceted biological roles and significance in the endothelial-mesenchymal transition (EndMT) during various fibrotic processes. However, the pathophysiological mechanisms linking vimentin to SARS-CoV-2 remain incompletely elucidated. In this study, we determined the expression profiles of vimentin in three cohorts: patients admitted to the intensive care unit with SARS-CoV-2 infection, individuals in the 6-12 month convalescent phase post-infection and COVID-19 negative controls. Our objective was to assess the association between peripheral blood biomarkers implicated in endothelial dysfunction and genes related to fibrosis. Serum levels of vimentin and N-cadherin were determined by ELISA, while vimentin gene expression was determined by qRT-PCR. In addition, we examined the correlation between clinical parameters and serum levels of vimentin and N-cadherin in severe COVID-19 patients and healthy counterparts. Our findings revealed elevated serum vimentin levels and increased gene expression in severe COVID-19 patients compared to healthy controls. Conversely, serum N-cadherin levels were diminished in both acute and convalescent stages of severe COVID-19 relative to healthy individuals. Notably, associations were observed between C-reactive protein, lactate dehydrogenase, lymphocyte count and vimentin levels in severe COVID-19 patients, indicative of endothelial dysfunction. Furthermore, our study identified vimentin and N-cadherin as potential diagnostic markers via ROC analysis. Overall, delineating the dysregulation of vimentin and N-cadherin due to SARS-CoV-2 infection in disease pathogenesis and tissue homeostasis offers novel insights for clinical management and targeted therapeutic interventions.