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Extracellular histones trigger oxidative stress-dependent induction of the NF-kB/CAM pathway via TLR4 in endothelial cells.

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Extracellular histones trigger oxidative stress-dependent induction of the NF-kB/CAM pathway via TLR4 in endothelial cells.

dc.contributor.author	Pérez Cremades, Daniel
dc.contributor.author	Bueno Betí, Carlos
dc.contributor.author	García Giménez, José Luis
dc.contributor.author	Ibáñez Cabellos, José Santiago
dc.contributor.author	Pallardó Calatayud, Federico Vicente
dc.contributor.author	Hermenegildo, Carlos
dc.contributor.author	Novella, Susana
dc.date.accessioned	2023-05-15T18:17:33Z
dc.date.available	2023-05-15T18:17:33Z
dc.date.issued	2022
dc.identifier.citation	Pérez Cremades, Daniel Bueno Betí, Carlos García Giménez, José Luis Ibáñez Cabellos, José Santiago Pallardó Calatayud, Federico Vicente Hermenegildo, Carlos Novella, Susana 2022 Extracellular histones trigger oxidative stress-dependent induction of the NF-kB/CAM pathway via TLR4 in endothelial cells. Journal of Physiology and Biochemistry
dc.identifier.uri	https://hdl.handle.net/10550/86620
dc.description.abstract	Extracellular histones have been reported to aggravate different pathophysiological processes by increasing vascular permeability, coagulopathy, and inflammation. In the present study, we elucidate how extracellular histones (10-100 mu g/mL) concentration dependently increase cytosolic reactive oxygen species (ROS) production using human umbilical vein endothelial cells (HUVECs). Furthermore, we identify cyclooxygenase (COX) and NADPH oxidase (NOX) activity as sources of ROS production in extracellular histone-treated HUVEC. This COX/NOX-mediated ROS production is also involved in enhanced NF-kB activity and cell adhesion molecules (VCAM1 and ICAM1) expression in histone-treated HUVEC. Finally, by using different toll-like receptor (TLR) antagonists, we demonstrate the role of TLR4 in CAMs overexpression triggered by extracellular histones in endothelial cells. In conclusion, our data suggest that through TLR4 signaling, extracellular histones increase endothelial cell activation, a mechanism involving increased COX- and NOX-mediated ROS. These findings increase our understanding on how extracellular histones enhance systemic inflammatory responses in diseases in which histone release occurs as part of the pathological processes.
dc.language.iso	eng
dc.relation.ispartof	Journal of Physiology and Biochemistry, 2022
dc.subject	Fisiologia cel·lular
dc.subject	Microorganismes patògens
dc.title	Extracellular histones trigger oxidative stress-dependent induction of the NF-kB/CAM pathway via TLR4 in endothelial cells.
dc.type	journal article
dc.date.updated	2023-05-15T18:17:33Z
dc.identifier.doi	10.1007/s13105-022-00935-z
dc.identifier.idgrec	158675
dc.rights.accessRights	open access