Amyloid precursor protein expression is induced by tumor necrosis factor alpha in 3T3-L1 adipocytes

J Cell Biochem. 2009 Dec 15;108(6):1418-22. doi: 10.1002/jcb.22382.

Abstract

Amyloid precursor protein (APP) has been characterized as an adipocyte-secreted protein that might contribute to obesity-related insulin resistance, inflammation, and dementia. In the current study, regulation of APP by the proinflammatory and insulin resistance-inducing cytokine tumor necrosis factor (TNF) alpha was determined in 3T3-L1 adipocytes. Interestingly, APP protein synthesis and mRNA expression were significantly increased by TNFalpha in a time-dependent manner with maximal induction observed after 24 h of treatment. Furthermore, TNFalpha induced APP mRNA expression dose-dependently with maximal 6.4-fold upregulation seen at 100 ng/ml effector. Moreover, inhibitor experiments suggested that TNFalpha-induced APP expression was mediated by nuclear factor kappa B. Taken together, we show for the first time a potent upregulation of APP by TNFalpha suggesting a potential role of this adipocyte-secreted protein in TNFalpha-induced insulin resistance and inflammatory disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Cell Proliferation
  • Mice
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Amyloid beta-Protein Precursor
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha