Study summary · research use only
Human cathelicidin peptide LL-37 induces endothelial-to-mesenchymal transition
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This in vitro study using human umbilical vein endothelial cells examined whether the cathelicidin peptide LL-37 induces endothelial-to-mesenchymal transition (EndMT), a process implicated in atherosclerotic plaques. The abstract reports LL-37 decreased endothelial cell markers and vascular network formation while increasing mesenchymal cell markers and cell migration. Blocking Akt and NF-κB inhibited the LL-37-induced EndMT, suggesting LL-37 acted through activation of Akt and NF-κB. The authors note LL-37 is localized in atherosclerotic plaques and describe the findings as raising the possibility of a role for LL-37 in atherosclerosis pathogenesis as an EndMT inducer.
Abstract
Endothelial-to-mesenchymal transition (EndMT) is a process that causes endothelial cells (ECs) to lose their EC characteristics and transform into mesenchymal cells. Accumulating studies suggest that EndMT is induced in atherosclerotic plaques and contributes to the pathogenesis of atherosclerosis. LL-37 is a multifaceted peptide with antimicrobial and immunomodulatory actions. Interestingly, LL-37 is localized in atherosclerotic plaques, suggesting an association between EndMT and LL-37 in atherosclerosis. Thus, we examined the EndMT-inducing activity of LL-37 using human umbilical vein ECs. LL-37 decreased EC markers but increased mesenchymal cell markers in the cells. LL-37 decreased the vascular network formation of the cells but increased the cell migration, a characteristic function of mesenchymal cells. Finally, the LL-37-induced EndMT was inhibited by Akt and nuclear factor-kappa B (NF-κB) inhibitors, suggesting that LL-37 induces EndMT by activating Akt and NF-κB. These observations speculate a role of LL-37 in the pathogenesis of atherosclerosis as an EndMT inducer.
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