Lactoferrin inhibits the inflammatory and angiogenic activation of bovine aortic endothelial cells

Mijung Yeom, Jongbong Park, Bombi Lee, Sang Yun Choi, Kyoung Soo Kim, Hyejung Lee, Dae Hyun Hahm

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Objective: Lactoferrin (Lf) is known to have anti-cancer and anti-inflammatory activities; however, its therapeutic mechanism has not been defined. In this study, to explain the therapeutic mechanism of Lf, we examined the effect of Lf on endothelial cell activation, leukocyte integration, and angiogenesis in vitro. Methods: Endothelia-leukocyte adhesion assays were used to assess primary cultures of bovine aortic endothelial cells (BAECs) activation following LPS treatment. The mRNA expression of ICAM-1 and proinflammatory cytokines was measured using RT-PCR. Each step of angiogenesis was evaluated in vitro, including endothelial cell proliferation, migration, and tube formation. Proliferation was examined using WST-1 and BrdU incorporation assays, while wound migration assays were used to evaluate cell migration; capillary-like tube formation assays on Matrigel were used to assess tube formation. Results: Lf reduced the adhesion of human monocyte-like THP-1 cells to BAECs by 45%. Lf also reduced mRNA expression of ICAM-1 and proinflammatory cytokines in BAECs. Lf significantly inhibited BAEC proliferation, migration, and tube formation. Conclusions: Lf exerted a potent effect on BAEC activation, suggesting that it might function via an endothelia-based mechanism in the treatment of various diseases, including rheumatoid arthritis and cancer.

Original languageEnglish
Pages (from-to)475-482
Number of pages8
JournalInflammation Research
Volume60
Issue number5
DOIs
Publication statusPublished - 2011 May

Keywords

  • Angiogenesis in vitro
  • Bovine aortic endothelial cells (BAEC)
  • Endothelium
  • Lactoferrin

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

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