Open Access

Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells

  • Authors:
    • Kaori Suzuki
    • Mari Ohkuma
    • Isao Nagaoka
  • View Affiliations

  • Published online on: July 31, 2019     https://doi.org/10.3892/ijmm.2019.4294
  • Pages: 1187-1196
  • Copyright: © Suzuki et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cellular senescence is associated with the induction of a proinflammatory phenotype. Notably, senescent endothelial cells are detected at the sites of atherosclerotic lesions, suggesting the involvement of senescent endothelial cells in atherogenesis. Moreover, bacterial infection has been speculated to contribute to the pathogenesis of atherosclerosis. The present study investigated the effects of Gram‑negative bacterial lipopolysaccharide (LPS) and LL‑37 (a human antimicrobial peptide of the cathelicidin family), on senescent endothelial cells, using serially passaged human endothelial cells. The results indicated that senescent endothelial cells exhibited the basal proinflammatory phenotype, as evidenced by higher intercellular adhesion molecule‑1 (ICAM‑1) expression and NF‑κB p65 phosphorylation, compared with non‑senescent cells. Additionally, exposure to LPS and LL‑37 further enhanced the expression of ICAM‑1 in senescent endothelial cells, compared with non‑senescent cells. Of note, the NF‑κB p65 pathway was more activated in senescent endothelial cells stimulated with LPS and LL‑37. Furthermore, the expression levels of the receptors for LPS and LL‑37 [toll‑like receptor 4 (TLR4) and purinergic receptor P2X 7 (P2X7), respectively] were upregulated in senescent endothelial cells. These observations indicated that LPS and LL‑37 enhanced the ICAM‑1 expression and NF‑κB p65 activation in senescent endothelial cells, potentially via the upregulated TLR4 and P2X7. Thus, senescent endothelial cells may contribute to the pathogenesis of atherosclerosis via the basal proinflammatory phenotype and the enhanced inflammatory responses against atherogenic factors, including LPS and LL‑37.

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October 2019
Volume 44 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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APA
Suzuki, K., Ohkuma, M., & Nagaoka, I. (2019). Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells. International Journal of Molecular Medicine, 44, 1187-1196. https://doi.org/10.3892/ijmm.2019.4294
MLA
Suzuki, K., Ohkuma, M., Nagaoka, I."Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells". International Journal of Molecular Medicine 44.4 (2019): 1187-1196.
Chicago
Suzuki, K., Ohkuma, M., Nagaoka, I."Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells". International Journal of Molecular Medicine 44, no. 4 (2019): 1187-1196. https://doi.org/10.3892/ijmm.2019.4294