Involvement of NEK2 and NEK9 in LPS - induced endothelial barrier dysfunction

Barabutis, Nektarios; Akhter, Mohammad S.

doi:10.1016/j.mvr.2023.104651

Cited by 1 publication

(2 citation statements)

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“…NEK2 can function in the cytoplasm as well as in the nucleus via localization modulation, due to alternative splicing. Moreover, it has recently been implicated in inflammatory processes [14,21].…”

Section: Discussionmentioning

confidence: 99%

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Protective Activities of Growth Hormone-Releasing Hormone Antagonists against Toxin-Induced Endothelial Injury

Fakir,

Barabutis

2024

Endocrines

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GHRH regulates the secretion of GH from the anterior pituitary gland, previously associated with cancer progression and inflammation. An emerging body of evidence suggests that GHRHAnt support endothelial barrier function, but the mechanisms mediating these events are not completely understood. In the present study, it is demonstrated that the GHRHAnt JV-1-36 counteracts barrier dysfunction due to LPS or LTA treatment in HUVECs, utilizing the Dextran–FITC assay. Moreover, it is shown in BPAECs that these bacterial toxins increase ROS generation, and that this effect is counteracted by JV-1-36, which reinstates the redox balance. The possible involvement of NEK2 in the beneficial activities of GHRHAnt in IFN-γ- and LPS-triggered hyperpermeability was also assessed, since that kinase is involved in inflammatory responses. NEK2 was increased in the inflamed cells, and JV-1-36 counteracted those endothelial events. Our data support the beneficial effects of GHRHAnt in toxin-induced endothelial injury.

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Section: Discussionmentioning

confidence: 99%

“…Furthermore, NEK2 was induced in the inflamed cells, and GHRHAnt counteracted those effects. Since NEK2 was previously linked to inflammatory responses, we introduce the possibility that this kinase is involved in the GHRHAnt-related beneficial effects in the endothelium [20,21].…”

Section: Introductionmentioning

confidence: 99%