Lipopolysaccharide-induced lung injury involves the nitration-mediated activation of RhoA.
MouseEndotoxin/LPSC57BL/6Male
Model: Lipopolysaccharide-induced acute lung injury; human lung microvascular endothelial cells challenged with LPS in vitro
NipR1 attenuated RhoA nitration and barrier disruption in LPS-challenged human lung microvascular endothelial cells, and in mice it attenuated vessel leakage and inflammatory cell infiltration and preserved lung function.
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