LRP1-Dependent BMPER Signaling Regulates Lipopolysaccharide-Induced Vascular Inflammation.

ABSTRACT:

Objective

Bacterial endotoxin (lipopolysaccharide)-mediated sepsis involves dysregulated systemic inflammation, which injures the lung and other organs, often fatally. Vascular endothelial cells act as both targets and mediators of lipopolysaccharide-induced inflammatory responses. Dysfunction of endothelium results in increases of proinflammatory cytokine production and permeability leakage. BMPER (bone morphogenetic protein-binding endothelial regulator), an extracellular modulator of bone morphogenetic protein signaling, has been identified as a vital component in chronic endothelial inflammatory responses and atherosclerosis. However, it is unclear whether BMPER also regulates inflammatory response in an acute setting such as sepsis. To address this question, we investigated th

SUBMITTER: Lockyer P 

PROVIDER: S-EPMC5532067 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature