NEK2 is involved in the mediation of the effects of LPS in endothelial cells

Endothelial impairment has been associated with cell and tissue dysfunction. In this study, we investigated the effects of never in mitosis gene A-related kinase 2 (NEK2) silencing in lipopolysaccharides (LPS) - induced injury in bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a). Our observations suggest that NEK2 silencing alleviates LPS-induced cofilin, myosin light chain 2 (MLC2), mitogen activated protein kinases (MAPKs), Janus kinase 2 (JAK2), signal transducer and activator of transcriptions (STATs) activation; and suppressed paracellular hyperpermeability, and reactive oxygen species (ROS) generation. Based on those findings, it is suggested that NEK2 is involved in the mediation of LPS-induced endothelial responses.