Lipopolysaccharides increase Kir2.1 expression in lung endothelial cells

Kir2.1 is an inwardly rectifying K⁺ channel that modulates membrane potential. It is expressed widely in smooth muscle, neurons, and endothelial cells. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe clinical syndromes, often causing the damage of epithelial and endothelial cells. Lipopolysaccharides (LPS) usually cause ALI/ARDS, directly or indirectly, and are used to reproduce the model in vivo. Here, we used differentially expressed gene analysis to find increasing Kir2.1 channel expression in human pulmonary microvascular endothelial cells cultured with LPS. Primary cultured mice pulmonary microvascular endothelial cells were verified by immunofluorescence. LPS incubation increased Kir2.1 channel expression in cultured mice pulmonary microvascular endothelial cells. A whole-cell voltage clamp was used to record the K⁺ current in cultured endothelial cells, showing increased whole-cell current in LPS treatment compared with controls. Additionally, the application of Ba²⁺, as an inhibitor of Kir2.1 channel, inhibited K⁺ current in both groups. We demonstrated that LPS may increase Kir2.1 channel expression in mice pulmonary microvascular endothelial cells to increase K⁺ flux, maintain hyperpolarization, and cause vasodilation, which may increase blood flow in pulmonary vessel bed, leading to pulmonary congestion contributing pneumonemia and ALI/ARDS.