eNOS, COX-2, and prostacyclin production are impaired in endothelial cells from diabetics

Chiara Bolego, Carola Buccellati, Tatjana Radaelli, Irene Cetin, Lina Puglisi, Giancarlo Folco, Angelo Sala

Research output: Contribution to journalArticlepeer-review


The vascular endothelium is a well-recognized target of damage for factors leading to increased cardiovascular risk. Among the agents playing an important role in cardiovascular homeostasis, nitric oxide and prostacyclin represent key markers of endothelial integrity. In the present work, we report for the first time the reduced expression of both endothelial nitric oxide synthase and cyclooxygenase-2 (COX-2) proteins, as well as decreased prostacyclin production, in unstimulated human endothelial cells from insulin-dependent diabetic mothers when compared to cells from non-diabetic, control subjects. According to a major role of COX-2 as a source of prostacyclin production even in unstimulated endothelial cells, prostacyclin production was concentration-dependently inhibited by the selective COX-2 inhibitor SC236. Overall, our results suggest a possible link between reduced endothelial COX-2 and NO-synthase expression and the increased risk of cardiovascular diseases affecting diabetic patients, and point to the use of endothelial cells from diabetic patients as a tool for investigating early dysfunction in pathological endothelium.

Original languageEnglish
Pages (from-to)188-190
Number of pages3
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - Jan 6 2006


  • COX-2
  • Endothelial cells
  • eNOS
  • Insulin-dependent diabetes
  • Prostacyclin

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


Dive into the research topics of 'eNOS, COX-2, and prostacyclin production are impaired in endothelial cells from diabetics'. Together they form a unique fingerprint.

Cite this