Glycoxidation of low-density lipoprotein promotes multiple apoptotic pathways and NFκB activation in human coronary cells

Filomena de Nigris, Lidia Gallo, Vincenzo Sica, Claudio Napoli

Research output: Contribution to journalArticlepeer-review

Abstract

Apoptosis of arterial cells induced by oxidized low-density lipoprotein (oxLDL) is thought to contribute to the progression of vascular dysfunction and atherogenesis. It is well established that diabetes mellitus is accompanied by both glycosylation and oxidation LDL, but the biological effects of these modified lipoproteins are poorly understood. We demonstrate here that glycosylated oxLDL (glc-oxLDL) promotes apoptotic signaling in human coronary smooth muscle cells. This was associated by a decrease of the antiapoptotic protein Bcl-2, an increase of the pro-apoptotic protein Bax, and activation of caspase 3. Glc-oxLDL also activated NFκB and decreased IκB, these effects were more pronounced than those achieved with oxLDL. Our study shows that glc-oxLDL influences a broad cascade of signaling transduction pathways, which may not only result in apoptosis, but also could affect NFκB in human coronary cells. This cascade of events may influence the evolution of atherogenesis and vascular complications in diabetic patients.

Original languageEnglish
Pages (from-to)101-108
Number of pages8
JournalBasic Research in Cardiology
Volume101
Issue number2
DOIs
Publication statusPublished - Mar 2006

Keywords

  • Atherosclerosis
  • Caspases
  • glc-oxLDL
  • NFκB
  • oxLDL

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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