Akt activation prevents Apop-1-induced death of cells

Biochem Biophys Res Commun. 2008 Dec 26;377(4):1097-101. doi: 10.1016/j.bbrc.2008.10.109. Epub 2008 Oct 31.

Abstract

Apop-1 is a novel protein identified in cultured atherosclerotic smooth muscle cells of ApoE-deficient mice, and the expression of the Apop-1 protein induces the death of cultured cells. Insulin-like growth factor-1 (IGF-1) is a well-characterized survival factor for VSMC; however, the interaction between Apop-1 and survival factor IGF-1 in the mediation of cell death is poorly understood. In this report, we show that the IGF-1 signaling cascade protects VSMC against Apop-1-induced death. Furthermore, our data indicate that the inhibition of Apop-1-induced death by IGF-1 is mediated by the activation of the PI3K/Akt signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins / metabolism*
  • Apoptosis*
  • Caspase 9 / metabolism
  • Cells, Cultured
  • Cytochromes c / metabolism
  • Enzyme Activation
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology
  • Mice
  • Mitochondria / drug effects
  • Mitochondria / enzymology
  • Mitochondrial Proteins / metabolism*
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism*

Substances

  • Apopt1 protein, mouse
  • Apoptosis Regulatory Proteins
  • Mitochondrial Proteins
  • insulin-like growth factor-1, mouse
  • Insulin-Like Growth Factor I
  • Cytochromes c
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Caspase 9