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
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis Regulatory Proteins / metabolism*
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Apoptosis*
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Caspase 9 / metabolism
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Cells, Cultured
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Cytochromes c / metabolism
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Enzyme Activation
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Insulin-Like Growth Factor I / metabolism
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Insulin-Like Growth Factor I / pharmacology
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Mice
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Mitochondria / drug effects
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Mitochondria / enzymology
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Mitochondrial Proteins / metabolism*
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Muscle, Smooth, Vascular / cytology*
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Muscle, Smooth, Vascular / drug effects
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Muscle, Smooth, Vascular / metabolism*
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Phosphatidylinositol 3-Kinases / metabolism
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Proto-Oncogene Proteins c-akt / metabolism*
Substances
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Apopt1 protein, mouse
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Apoptosis Regulatory Proteins
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Mitochondrial Proteins
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insulin-like growth factor-1, mouse
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Insulin-Like Growth Factor I
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Cytochromes c
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Phosphatidylinositol 3-Kinases
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Proto-Oncogene Proteins c-akt
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Caspase 9