β2-adrenoceptor stimulation inhibits advanced glycation end products-induced adhesion molecule expression and cytokine production in human peripheral blood mononuclear cells

Hideo Kohka Takahashi, Shuji Mori, Keyue Liu, Hidenori Wake, Jiyong Zhang, Rui Liu, Tadashi Yoshino, Masahiro Nishibori

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Cell-to-cell interaction through binding of intercellular adhesion molecule-1 (ICAM-1) and CD40 on monocytes to their ligands on T-cells plays crucial roles in cytokine production. Advanced glycation end products (AGEs) subtypes induce complications in diabetes. In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 μg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-γ and tumor necrosis factor (TNF)-α in human peripheral blood mononuclear cells. β2-adrenoceptor stimulation has been demonstrated to modulate the production of inflammatory mediators. In the present study, we found that norepinephrine, epinephrine and isoproterenol inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production in a concentration-dependent manner. The action of these catecholamines was antagonized by β2-adrenoceptor antagonist, but not by α1-, α2- and β1-adrenoceptor antagonist. β2-adrenoceptor agonists, salbutanol and terbutaline inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production, but α1-, α2- and β1-adrenoceptor agonist had no effect, indicating that the stimulation of β2-adrenoceptor might improve AGEs-initiated complications in diabetes.

Original languageEnglish
Pages (from-to)313-317
Number of pages5
JournalEuropean Journal of Pharmacology
Volume627
Issue number1-3
DOIs
Publication statusPublished - Feb 10 2010

Keywords

  • Adhesion molecule
  • Advanced glycation end product
  • Monocyte
  • β-adrenoceptor

ASJC Scopus subject areas

  • Pharmacology

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