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ABSTRACT: Background
During infectious diseases, proinflammatory cytokines transiently destabilize interactions between adjacent vascular endothelial cells (ECs) to facilitate the passage of immune molecules and cells into tissues. However, in the lung, the resulting vascular hyperpermeability can lead to organ dysfunction. Previous work identified the transcription factor ERG (erythroblast transformation-specific-related gene) as a master regulator of endothelial homeostasis. Here we investigate whether the sensitivity of pulmonary blood vessels to cytokine-induced destabilization is due to organotypic mechanisms affecting the ability of endothelial ERG to protect lung ECs from inflammatory injury.Methods
Cytokine-dependent ubiquitination and proteasomal degradation of ERG were anal
SUBMITTER: Schafer CM
PROVIDER: S-EPMC10364964 | biostudies-literature | 2023 Aug
REPOSITORIES: biostudies-literature