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Título

Compensatory increase of VE-cadherin expression through ETS1 regulates endothelial barrier function in response to TNF¿

AutorCaballero, Álvaro; Ribas, Catalina CSIC ORCID; Correas, Isabel CSIC ORCID; Colás-Algora, Natalia; García-Weber, Diego CSIC ORCID; Cacho-Navas, Cristina; Barroso, Susana CSIC; Millán, Jaime CSIC ORCID
Palabras claveEndothelial barrier function
Permeability
VE-cadherin
NF-κB
ETS1
LPS
Resolution of inflammation
Adherens junctions
Degradation
Fecha de publicación8-ago-2019
EditorBirkhäuser Verlag
CitaciónCellular and Molecular Life Sciences 71 (2020)
ResumenVE-cadherin plays a central role in controlling endothelial barrier function, which is transiently disrupted by proinflammatory cytokines such as tumor necrosis factor (TNFα). Here we show that human endothelial cells compensate VE-cadherin degradation in response to TNFα by inducing VE-cadherin de novo synthesis. This compensation increases adherens junction turnover but maintains surface VE-cadherin levels constant. NF-κB inhibition strongly reduced VE-cadherin expression and provoked endothelial barrier collapse. Bacterial lipopolysaccharide and TNFα upregulated the transcription factor ETS1, in vivo and in vitro, in an NF-κB dependent manner. ETS1 gene silencing specifically reduced VE-cadherin protein expression in response to TNFα and exacerbated TNFα-induced barrier disruption. We propose that TNFα induces not only the expression of genes involved in increasing permeability to small molecules and immune cells, but also a homeostatic transcriptional program in which NF-κB- and ETS1-regulated VE-cadherin expression prevents the irreversible damage of endothelial barriers
URIhttp://hdl.handle.net/10261/235651
Identificadoresissn: 1420-9071
Aparece en las colecciones: (CBM) Artículos




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