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In vitro study demonstrates that NEK2 knockdown reduces barrier disruption and inflammation in pulmonary endothelial cells, suggesting a key therapeutic target for endothelial dysfunction.
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.
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Sarker et al. (2026) studied this question.
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