Lymphotoxin-α3 mediates monocyte-endothelial interaction by TNFR I/NF-κB signaling

Shinichiro Suna, Yasuhiko Sakata, Masahiko Shimizu, Daisaku Nakatani, Masaya Usami, Sen Matsumoto, Hiroya Mizuno, Kouichi Ozaki, Seiji Takashima, Hiroshi Takeda, Toshihiro Tanaka, Masatsugu Hori, Hiroshi Sato

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


We recently reported that the single nucleotide polymorphisms of the lymphotoxin-(LT)α gene, a member of the tumor necrosis factor (TNF) family, are closely related to acute myocardial infarction; however, the precise mechanism of LTα signaling in atherogenesis remains unclear. We investigated the role of LTα3, a secreted homotrimer of LTα, in monocyte-endothelial cell adhesion using cultured human umbilical vein endothelial cells (HUVEC). We found that LTα3 induced cell adhesion molecules and activated NF-κB p50 and p65. LTα3 also induced phosphorylation of Akt, phosphorylation and degradation of IκB, nuclear translocation of p65, and increased adhesion of THP1 monocytes to HUVEC. These effects were mediated by TNF receptor (TNFR) I and attenuated by the phosphatidylinositol triphosphate-kinase (PI3K) inhibitors LY294002 and Wortmannin. Thus, LTα3 mediates the monocyte-endothelial interaction via the classical NF-κB pathway following TNFR I/PI3K activation, indicating it may play a role in the development of coronary artery disease.

Original languageEnglish
Pages (from-to)374-378
Number of pages5
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2009 Feb 6
Externally publishedYes


  • Atherosclerosis
  • Cell adhesion molecule
  • Lymphotoxin-α
  • NF-κB
  • TNF receptor

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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