Endothelial transcriptomic, epigenomic and proteomic data challenge the proposed role for TSAd in vascular permeability.

ABSTRACT: The vascular endothelial growth factor VEGF drives excessive vascular permeability to cause tissue-damaging oedema in neovascular and inflammatory diseases across multiple organs. Several molecular pathways have been implicated in VEGF-induced hyperpermeability, including binding of the VEGF-activated tyrosine kinase receptor VEGFR2 by the T-cell specific adaptor (TSAd) to recruit a SRC family kinase to induce junction opening between vascular endothelial cells (ECs). Inconsistent with a universal role for TSAd in permeability signalling, immunostaining approaches previously reported TSAd only in dermal and kidney vasculature. To address this discrepancy, we have mined publicly available omics data for expression of TSAd and other permeability-relevant signal transducers in multiple organs

SUBMITTER: Brash JT 

PROVIDER: S-EPMC11906500 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature