Glimepiride activates eNOS with a mechanism Akt but not caveolin-1 dependent

Barbara Salani, Silvia Repetto, Renzo Cordera, Davide Maggi

Research output: Contribution to journalArticlepeer-review


Insulin stimulates caveolin-1 and eNOS phosphorylation. The sulfonylurea glimepiride mimics several insulin actions by mechanisms that are poorly understood. Glimepiride induces caveolin-1 phosphorylation and activates PI3K and Akt in rat adipocytes. In this paper, we investigated the effect of glimepiride on eNOS activation in human endothelial cells. We found that glimepiride induces caveolin-1 and eNOS phosphorylation. To better understand the role of caveolin-1 in glimepiride action, we downregulated caveolin-1 expression by specific siRNA transfection. Caveolin-1 silencing did not change eNOS and Akt phosphorylation induced by glimepiride. On the contrary, LY294002, a specific PI3K inhibitor, blocked eNOS serine 1177 phosphorylation. These findings suggest that glimepiride induces eNOS phosphorylation in endothelial cells through an Akt-dependent mechanism, not regulated by caveolin-1.

Original languageEnglish
Pages (from-to)832-835
Number of pages4
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Sep 30 2005


  • Akt
  • Caveolin-1
  • eNOS
  • Glimepiride

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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