Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...

Details

Autor(en) / Beteiligte
Titel
Insulin‐like growth factor‐1 and TNF‐α regulate autophagy through c‐jun N‐terminal kinase and Akt pathways in human atherosclerotic vascular smooth cells
Ist Teil von
  • Immunology and cell biology, 2006-10, Vol.84 (5), p.448-454
Ort / Verlag
Nature Publishing Group
Erscheinungsjahr
2006
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • A balance between programmed cell death and survival of vascular smooth muscle cells (VSMC) in the fibrous cap, which is primarily composed of VSMC and extracellular matrix, appears to best correlate with plaque instability or stability and is controlled by growth factors and cytokines. Autophagy is also involved in programmed cell death. We assessed the effect of TNF‐α and insulin‐like growth factor‐1 (IGF‐1) on the expression of autophagic genes, microtubule‐associated protein 1 light chain 3 (MAPLC‐3) and Beclin‐1 in VSMC isolated from atherosclerotic plaques. Transmission electron microscopy showed a significantly higher number of vacuolated cells in the TNF‐α‐treated VSMC and a markedly lower number in the IGF‐1‐treated VSMC when compared with the untreated control group. TNF‐α‐induced MAPLC‐3 mRNA expression through c‐jun N‐terminal kinase and protein kinase B pathways and induced Beclin‐1 protein expression through the c‐jun N‐terminal kinase pathway. Expression of MAPLC‐3 and Beclin‐1 correlated with autophagic cell death of plaque VSMC. IGF‐1 inhibited MAPLC‐3 mRNA transcripts through the Akt pathway. These findings suggest that the expression of autophagy genes can be influenced by IGF‐1 and TNF‐α through c‐jun N‐terminal kinase or Akt pathways and autophagy might be involved in the regulation of plaque stability.
Sprache
Englisch
Identifikatoren
ISSN: 0818-9641
eISSN: 1440-1711
DOI: 10.1111/j.1440-1711.2006.01454.x
Titel-ID: cdi_proquest_miscellaneous_68807879

Weiterführende Literatur

Empfehlungen zum selben Thema automatisch vorgeschlagen von bX