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September 15, 2026Tissue Barriers

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

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Authors

MSMd Matiur Rahman SarkerSFSaikat FakirMSMadan Sigdel

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Overview

In vitro study demonstrates that NEK2 knockdown reduces barrier disruption and inflammation in pulmonary endothelial cells, suggesting a key therapeutic target for endothelial dysfunction.

Key Points

  • To examine the therapeutic impact of NEK2 silencing on lipopolysaccharide (LPS)-induced injury in pulmonary endothelial cells.
  • Silenced NEK2 in bovine pulmonary artery endothelial cells (BPAEC) and human lung microvascular endothelial cells (HULEC-5a).
  • Exposed cells to LPS and evaluated intracellular inflammatory signaling cascades, barrier permeability, and reactive oxygen species generation.
  • NEK2 knockdown attenuated LPS-induced activation of cofilin, myosin light chain 2 (MLC2), MAPKs, and JAK2/STAT signaling pathways.
  • NEK2 silencing significantly suppressed LPS-triggered paracellular hyperpermeability and reactive oxygen species (ROS) production.

Cite This Study

Sarker et al. (2026) studied this question.

synapsesocial.com/papers/6aa913d99013453be30a2055https://doi.org/10.1080/21688370.2026.2732890
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