title: ROS-activated calcium signaling mechanisms regulating endothelial barrier function.
abstract: Increased vascular permeability is a common pathogenic feature in many inflammatory diseases. For example in acute lung injury (ALI) and its most severe form, the acute respiratory distress syndrome (ARDS), lung microvessel endothelia lose their junctional integrity resulting in leakiness of the endothelial barrier and accumulation of protein rich edema. Increased reactive oxygen species (ROS) generated by neutrophils (PMNs) and other inflammatory cells play an important role in increasing endothelial permeability. In essence, multiple inflammatory syndromes are caused by dysfunction and compromise of the barrier properties of the endothelium as a consequence of unregulated acute inflammatory response. This review focuses on the role of ROS signaling in controlling endothelial permeability with particular focus on ALI. We summarize below recent progress in defining signaling events leading to increased endothelial permeability and ALI.
authors.affiliation: Department of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States.
authors.forename: Anke
authors.initials: A
authors.lastname: Di
authors.affiliation: Department of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States.
authors.forename: Dolly
authors.initials: D
authors.lastname: Mehta
authors.affiliation: Department of Pharmacology, The University of Illinois College of Medicine, Chicago, IL 60612, United States. Electronic address: abmalik@uic.edu.
authors.forename: Asrar B
authors.initials: AB
authors.lastname: Malik
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D002199:Capillary Permeability; D002463:Cell Membrane Permeability; D004727:Endothelium / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species